Vascular system

VASCULAR SYSTEM

THE term vascular system designates all the arrangements in the body connected with the circulation of the blood. A description of the anatomy of the various organs as found in man is given under Anatomy (vol. i. p. 899 sq.), and an account of various modifications of the circulatory apparatus under the headings designating the great groups of the animal kingdom, such as Mollusca, Crustacea, Ichthyology, Amphibia, Reptiles, Birds; and reference may be made to the articles Nutrition and Respiration for details as to the formation, physical and chemical properties, and functions of the blood. The present article is devoted to a consideration of the mechanism by which the circulation is carried on in the Mammalia and in man, a branch of physiology which has been more successfully investigated than any other department of the science.

Historical Sketch.

Galen, following Erasistratus and Aristotle, clearly dis- .nguished arteries from veins, and was the first to overthrow the old theory of Erasistratus that the arteries contained air. According to him, the vein arose from the liver in two great trunks, the vena porta and vena cava. The first was formed by the union of all the abdominal veins, which absorbed the chyle prepared in the stomach and intestines, and carried it to the liver, where it was converted into blood. The vena cava arose in the liver, divided into two branches, one ascending through the diaphragm to the heart, furnishing the proper veins of this organ; there it received the vena azygos, and entered the right ventricle, along with a large trunk from the lungs, evidently the pulmonary artery. The vena azygos was the superior vena cava, the great vein which carries the venous blood from the head and upper extremities into the right auricle. The descending branch of the great trunk supposed to originate in the liver was the inferior vena cava, below the junction of the hepatic vein. The arteries arose from the left side of the heart by two trunks, one having thin walls, the pulmonary veins, the other having thick walls, the aorta. The first was supposed to carry blood to the lungs, and the second to carry blood to the body. The heart consisted of two ventricles, communicating by pores in the septum; the lungs were parenchymatous organs communicating with the heart by the pulmonary veins. The blood-making organ, the liver, separates from the blood subtle vapours, the natural spirits, which, carried to the heart, mix with the air introduced by respiration, and thus form the vital spirits ; these, in turn carried to the brain, are elaborated into animal spirits, which are distributed to all parts of the body by the nerves. Such were the views of Galen, taught until early in the 16th century.

Jacobus Berengarius of Carpi (ob. 1527) investigated the structure of the valves of the heart. Andreas Vesale or Vesalius (1514-1564) contributed largely to anatomical knowledge, especially to the anatomy of the circulatory organs. He determined the position of the heart in the chest; he studied its structure, pointing out the fibrous rings at the bases of the ventricles; he showed that its wall consists of layers of fibres connected with the fibrous rings; and he described these layers as being of three kinds,—straight or vertical, oblique, and circular or transverse. From the disposition of the fibres he reasoned as to the mechanism of the contraction and relaxation of the heart. He supposed that the relaxation, or diastole, was accounted for principally by the longitudinal fibres contracting so as to draw the apex towards the base, and thus cause the sides to bulge out; whilst the contraction, or systole, was due to contraction of the transverse or oblique fibres. He showed that the pores of Galen, in the septum between the ventricles, did not exist, so that there could be no communication between the right and left sides of the heart, except by the pulmonary circulation. He also investigated minutely the internal structure of the heart, describing the valves, the columnae carneae, and the musculi papillares. He described the mechanism of the valves with much accuracy. He had, however, no conception either of a systemic or of a pulmonary circulation. To him the heart was a reservoir from which the blood ebbed and flowed, and there were two kinds of bloo*d, arterial and venous, having different circulations and serving different purposes in the body. Vesalius was not only a great anatomist: he was a great teacher; and his pupils carried on the work in the spirit of their master. Prominent among them was Gabriel Fallopius (1523-1562), who studied the anastomoses of the blood-vessels, without the art of injection, which was invented by Frederick Ruysch (1638-1731) more than a century later. Another pupil was Columbus (Matthieu Reald Columbo, ob. 1559), first a prosector in the anatomical rooms of Vesalius and afterwards his successor in the chair of anatomy in Padua; his name has been mentioned as that of one who anticipated Harvey in the discovery of the circulation of the blood. A study of his writings clearly shows that he had no true knowledge of the circulation, but only a glimpse of how the blood passed from the right to the left side of the heart. In his work there is evidently a sketch of the pulmonary circulation, although it is clear that he did not understand the mechanism of the valves, as Vesalius did. As regards the systemic circulation, there is the notion simply of an oscillation of the blood from the heart to the body and from the body to the heart. Further, he upholds the view of Galen, that all the veins originate in the liver; and he even denies the muscular structure of the heart. In 1553 Michael Servetus (1511-1553), a pupil or junior fellow-student of Vesalius, in his Christianismi Restitutio, described accurately the pulmonary circulation. Servetus perceived the course of the circulation from the right to the left side of the heart through the lungs, and he also recognized that the change from venous into arterial blood took place in the lungs and not in the left ventricle. Not so much the recognition of the pulmonary circulation, as that had been made previously by Columbus, but the discovery of the respiratory changes in the lungs constitutes Servetus’s claim to be a pioneer in physiological science.

Andrea Cesalpino (1519-1603), a great naturalist of this period, also made important contributions towards the discovery of the circulation, and in Italy he is regarded as the real discoverer. Cesalpinus knew the pulmonary circulation. Further, he was the first to use the term “circulation,” and he went far to demonstrate the systemic circulation. He experimentally proved that, when a vein is tied, it fills below and not above the ligature. The following passage from his Quaestiones Medicae, (lib. v., cap. 4, fol. 125), quoted by Gamgee, shows his views :—

“The lungs, therefore, drawing the warm blood from the right ventricle of the heart through a vein like an artery, and returning it by anastomosis to the venal artery (pulmonary vein), which tends towards the left ventricle of the heart, and air, being in the meantime transmitted through the channels of the aspera arteria (trachea and bronchial tubes), which are extended near the venal artery, yet not communicating with the aperture as Galen thought, tempers with a touch only. This circulation of the blood (huic sanguinis circulationi) from the right ventricle of the heart through the lungs into the left ventricle of the same exactly agrees with what appears from dissection. For there are two receptacles ending in the right ventricle and two in the left. But of the two only one intromits; the other lets out, the membranes (valves) being constituted accordingly.”

Still Cesalpinus clung to the old idea of there being an efflux and reflux of blood to and from the heart, and he had confused notions as to the veins conveying nutritive matter, whilst the arteries carried the vital spirits to the tissues. He does not even appear to have thought of the heart as a contractive and propulsive organ, and attributed the dilatation to “an effervescence of the spirit,” whilst the contraction,—or, as he termed it, the “collapse,”—was due to the appropriation by the heart of nutritive matter. Whilst he imagined a communication between the termination of the arteries and the commencement of the veins, he does not appear to have thought of a direct flow of blood from the one to the other. Thus he cannot be regarded as the true discoverer of the circulation of the blood. More recently Ercolani has put forward claims on behalf of Carlo Ruini as being the true discoverer. Ruini published the first edition of his anatomical writings in 1598, the year William Harvey entered at Padua as a medical student. This claim has been carefully investigated by Gamgee, who has come to the conclusion that it cannot be maintained.

The anatomy of the heart was examined, described, and figured by Bartolomeo Eustacheo (c . 1500-1574) and by Julius Caesar Aranzi or Arantius (c . 1530-1589), whose name is associated with the fibro-cartilaginous thickenings on the free edge of the semilunar valves (corpora Arantii). Hieronymus Fabricius of Acquapendente (1537-1619), the immediate predecessor and teacher of Harvey, made the important step of describing the valves in the veins; but he thought they had a subsidiary office in connexion with the collateral circulation, supposing that they diverted the blood into branches near the valves; thus he missed seeing the importance of the anatomical and experimental facts gathered by himself. At the time when Harvey arose the general notions as to the circulation may be briefly summed up as follows: the blood ebbed and flowed to and from the heart in the arteries and veins; from the right side at least a portion of it passed to the left side through the vessels in the lungs, where it was mixed with air; and, lastly, there were two kinds of blood,—the venous, formed originally in the liver, and thence passing to the heart, from which it went out to the periphery by the veins and returned by those to the heart, and the arterial,—containing “spirits” produced by the mixing of the blood and the air in the lungs—sent out from the heart to the body and returning to the heart by the same vessels. The pulmonary circulation was understood so far, but its relation to the systemic circulation was unknown. The action of the heart, also, as a propulsive organ was not recognized. It was not until 1628 that Harvey announced his views to the world by publishing his treatise De Motu Cordis et Sanguinis (see vol. xi. pp. 503-504). His conclusions are given in the following celebrated passage :—

“And now I may be allowed to give in brief my view of the circulation of the blood, and to propose it for general adoption. Since all things, both argument and ocular demonstration, show that the blood passes through the lungs and heart by the auricles and ventricles, and is sent for distribution to all parts of the body, where it makes its way into the veins and pores of the flesh, and then flows by the veins from the circumference on every side to the centre, from lesser to the greater veins, and is by them finally discharged into the vena cava and right auricle of the heart, and this in such a quantity, or in such a flux and reflux, thither by the arteries, hither by the veins, as cannot possibly be supplied by the ingestor, and is much greater than can be required for mere purposes of nutrition, it is absolutely necessary to conclude that the blood in the animal body is impelled in a circle, and is in a state of ceaseless motion, that this is the act or function which the heart performs by means of its pulse, and that it is the sole and only end of the motion and contraction of the heart” (bk. x. ch. xiv. p. 68).

Opposed by Caspar Hofmann of Nuremberg, Veslingius of Padua, and J. Riolanus the younger, this new theory was supported by Roger Drake, a young Englishman, who chose it for the subject of a graduation thesis at Leyden in 1637, by Rolfink of Jena, and especially by Descartes, and quickly gained the ascendant; and its author had the satisfaction of seeing it confirmed by the discovery of the capillary circulation, and universally adopted. The circulation in the capillaries between the arteries and the veins was discovered by Marcellus Malpighi (1628-1694) of Bologna in 1661. He saw it first in the lungs and the mesentery of a frog, and the discovery was announced in the second of two letters, Epistola de Pulmonibus, addressed to Borelli, and dated 1661. Malpighi actually showed the capillary circulation to the astonished eyes of Harvey. Anthony van Leeuwenhoek (1632-1723) in 1673 repeated Malpighi’s observations, and studied the capillary circulation in a bat’s wing, the tail of a tadpole, and the tail of a fish. William Molyneux studied the circulation in the lungs of a water newt in 1683.

The idea that the same blood was propelled through the body in a circuit suggested that life might be sustained by renewing the blood in the event of some of it being lost. About 1660 Lower, a London physician (died 1691), succeeded in transferring the blood of one animal directly from its blood-vessels into those of another animal. This was first done by passing a “quill” or a “small crooked pipe of silver or brass” from the carotid artery of one dog to the jugular vein of another. This experiment was repeated and modified by Sir Edmund King, Coxe, Gayant, and Denys with such success as to warrant the operation being performed on man, and accordingly it was carried out by Lower and King on 23d November 1667, when blood from the arteries of a sheep was directly introduced into the veins of a man. It would appear that the operation had previously been performed with success in Paris.

The doctrine of the circulation being accepted, physiologists next directed their attention to the force of the heart, the pressure of the blood in the vessels, its velocity, and the phenomena of the pulse wave. Giovanni Alphonso Borelli (1608-1679) investigated the circulation during the lifetime of Harvey. He early conceived the design of applying mathematical principles to the explanation of animal functions; and, although he fell into many errors, he must be regarded as the founder of animal mechanics. In his De Motu Animalium (1680-85) he stated his theory of the circulation in eighty propositions, and in prop. lxxiii., founding on a supposed relation between the bulk and the strength of muscular fibre as found in the ventricles, erroneously concluded that the force of the heart was equal to the pressure of a weight of 180,000 lb. He also recognized and figured the spiral arrangement of fibres in the ventricles. The question was further investigated by James Keill, a Scottish physician (1673-1719), who in his Account of Animal Secretion, the Quantity of Blood in the Human Body, and Muscular Motion (1708) attempted to estimate the velocity of blood in the aorta, and gave it at 52 feet per minute. Then, allowing for the resistance of the vessels, he showed that the velocity diminishes towards the smaller vessels, and arrived at the amazing conclusion that in the smallest vessels it travels at the rate of ¼ inch in 278 days,—a good example of the extravagant errors made by the mathematical physiologists of the period. Keill further described the hydraulic phenomena of the circulation in papers communicated to the Royal Society and collected in his Essays on Several Parts of the Animal (Economy (1717). In these essays, by estimating the quantity of blood thrown out of the heart by each contraction, and the diameter of the aortic orifice, he calculated the velocity of the blood. He stated (pp. 84, 87) that the blood sent into the aorta with each contraction would form a cylinder 8 inches (2 ounces) in length and be driven along with a velocity of 156 feet per minute. Estimating then the resistances to be overcome in the vessels, he found the force of the heart to be “little above 16 ounces,”—a remarkable difference from the computation of Borelli. Keill’s method was ingenious, and is of historical interest as being the first attempt to obtain quantitative results; but it failed to obtain true results, because the data on which he based his calculations were inaccurate. These calculations attracted the attention not only of the anatomico-physiologists, such as Haller, but also of some of the physicists of the time, notably of Jurin and D. Bernoulli. Jurin (died 1750) gave the force of the left ventricle at 9 lb 1 oz. and that of the right ventricle at 6 lb 3 oz. He also stated with remarkable clearness, considering that he reasoned on the subject as a physicist, without depending on experimental data gathered by himself, the influence on the pulse induced by variations in the power of the heart or in the resistance to be overcome. The experimental investigation of the problem was supplied by Stephen Hales (1677-1761), rector of Teddington in Middlesex, who in 1708 devised the method of estimating the force of the heart by inserting a tube into a large artery and observing the height to which the blood was impelled into it. Hales is the true founder of the modern experimental method in physiology. He observed in a horse that the blood rose in the vertical tube, which he had connected with the crural artery, to the height of 8 feet 3 inches perpendicular above the level of the left ventricle of the heart. But it did not attain its full height at once: it rushed up about half way in an instant, and afterwards gradually at each pulse 12, 8, 6, 4, 2, and sometimes 1 inch. When it was at its full height, it would rise and fall at and after each pulse 2, 3, or 4 inches; and sometimes it would fall 12 or 14 inches, and have there for a time the same vibrations up and down at and after each pulse as it had when it was at its full height, to which it would rise again after forty or fifty pulses. He then estimated the capacity of the left ventricle by a method of employing waxen casts, and, after many such experiments and measurements in the horse, ox, sheep, fallow deer, and dog, he calculated that the force of the left ventricle in man is about equal to that of a column of blood 7½ feet high, weighing 51 ½ lb, or, in other words, that the pressure the left ventricle has to overcome is equal to the pressure of that weight. When we contrast the enormous estimate of Borelli (180,000 R») with the underestimate of Keill (16 oz.), and when we know that the estimate of Hales, as corroborated by recent investigations by means of elaborate scientific appliances, is very near the truth, we recognize the far higher service rendered to science by careful and judicious experiment than by speculations, however ingenious. With the exception of some calculations by Dan Bernoulli in 1748, there was no great contribution to haemadynamics till 1808, when two remarkable papers appeared from Thomas Young (1773- 1829). In the first, entitled “Hydraulic Investigations,” which appeared in the Phil. Trans., he investigated the friction and discharge of fluids running in pipes and the velocity of rivers, the resistance occasioned by flexures in pipes and rivers, the propagation of an impulse through an elastic tube, and some of the phenomena of pulsations. This paper was preparatory to the second, “On the Functions of the Heart and Arteries,”—the Croonian lecture for 1808—in which he showed more clearly than had hitherto been done (1) that the blood-pressure gradually diminishes from the heart to the periphery; (2) that the velocity of the blood becomes less as it passes from the greater to the smaller vessels; (3) that the resistance is chiefly in the smaller vessels, and that the elasticity of the coats of the great arteries comes into play in overcoming this resistance in the interval between systoles; and (4) that the contractile coats do not act as propulsive agents, but assist in regulating the distribution of blood.

The next epoch of physiological investigation is characterized by the introduction of instruments for accurate measurement, and the graphic method of registering phenomena, now so largely used in science. In 1825 appeared E. and W. Weber’s Wellenlehre, and in 1838 E. Weber’s Ad Notat. Anatom. et Physiolog., i., both of which contain an exposition of E. H. Weber’s schema of the circulation, a scheme which presents a true and consistent theory. In 1826 Poiseuille invented the haemadynamometer. This was adapted with a marker to a recording cylinder by Ludwig in 1847, so as to form the instrument named by Volkmann the kymograph. Volkmann devised the haema-dromometer for measuring the velocity of the blood in 1850; for the same purpose Vierordt constructed the haematachometer in 1858; Chauveau and Lortet first used their haemadromograph in 1860; and lastly, Ludwig and Dogiel obtained the best results as regards velocity by the “stream-clock” in 1867. As regards the pulse, the first sphygmograph was constructed by Vierordt in 1856; and Marey’s form, of which there are now many modifications, appeared in 1860. In 1861 Chauveau and Marey obtained tracings of the variations of pressure in the heart cavities (see p. 99 below) by an experiment which is of great historical importance. During the past twenty-five years vast accumulations of facts have been made through the instruments of precision above alluded to, so that the conditions of the circulation, as a problem in hydrodynamics, have been thoroughly investigated. Since 1845, when the brothers Weber discovered the inhibitory action of the vagus, and 1858, when Claude Bernard formulated his researches showing the existence of a vaso-motor system of nerves, much knowledge has been acquired as to the relations of the nervous to the circulatory system. The Webers, John Reid, Claude Bernard, and Carl Ludwig may be regarded as masters in physiology equal in standing to those whose researches have been more especially alluded to in this historical sketch. The Webers took the first step towards recognizing the great principle of inhibitory action; John Reid showed how to investigate the functions of nerves by his classical research on the eighth pair of cranial nerves; Claude Bernard developed the fundamental conception of vaso-motor nerves; and Ludwig showed how this conception, whilst it certainly made the hydraulic problems of the circulation infinitely more complicated than they were even to the scientific imagination of Thomas Young, accounted for some of the phenomena and indicated at all events the solidarity of the arrangements in the living being. Further, Ludwig and his pupils used the evidence supplied by some of the phenomena of the circulation to explain even more obscure phenomena of the nervous system, and they taught pharmacologists how to study in a scientific manner the physiological action of drugs.

Physiology, &c., of Circulation.

The blood is contained during life in a continuous system of more or less elastic and contractile vessels. These are (1) the arteries, terminating in (2) the capillaries, from which originate (3) the veins, whilst a special contractile organ, (4) the heart, is placed at the commencement of the arteries and the termination of the veins (see fig. 1). The heart may be regarded as a double organ, each half consisting of an auricle and a ventricle, the right half containing blood which has been returned from the body to be sent to the lungs, and the left half containing blood which has been returned from the lungs to be distributed to the body. There are thus, in a sense, two circulations,—the one pulmonary, from the right side of the heart, by the pulmonary artery to the lungs, through the capillaries of the lungs, and back to the left side of the heart by the pulmonary veins, and the other systemic, from the left side of the heart, by the aorta, and the arteries which ramify from it, to 4he capillaries throughout the tissues, and from thence by the veins to the right side of the heart. Thus the course of the circulation may be traced

(1) from right auricle to right ventricle, through the right auriculo-ventricular opening, guarded by the tricuspid valve;

(2) from right ventricle by the pulmonary artery, through the capillaries of the lungs, to the pulmonary veins, which open into the left auricle; (3) from left auricle to left ventricle, through the left auriculo-ventricular opening, guarded by the mitral valve; (4) from the left ventricle through the greater arteries, the medium-sized arteries, and the arterioles into the capillaries of the tissues and organs; and (5) from thence by the veins, opening into larger and larger trunks, so as ultimately to constitute the superior and inferior venae cavae, which open into the right auricle, the point from which we started. Remembering that the walls of these tubes are all more or less elastic, imagine them to be distended with blood; there would then be a condition of permanent tension, which would be varied if pressure were applied to any part of the system. Such a variation of pressure would produce a movement of the fluid in the direction of less pressure, and, as the fluid cannot escape, there would be a circulation, which would be carried in the same direction by mechanical arrangements of valves. In the living body the contractions of the heart force blood into the arterial system and increase the pressure in that part of the circulation; the arteries empty part of their contents into the capillaries, which cany the blood to the veins, so as to tend to an equalization of pressure between the venous and arterial systems. If the pressure in both systems became equal, there would be no circulation; but, as the veins pour a portion of the blood back again into the heart, this organ on being refilled again contracts, forcing more blood into the arterial system and again raising the pressure there; thus the possibility during life of an equalization of arterial and venous pressure is prevented. In describing more fully the mechanism by which this circulation is maintained we shall consider (1) the action of the heart, and (2) the action of the blood-vessels, arteries, capillaries, and veins.

The Action of the Heart.

The form, position, and general arrangements of the heart are described under Anatomy (vol. i. pp. 899-908), and it is only necessary here to allude to certain points of physiological importance.

The substance of the heart is composed of a special variety of muscular tissue, along with connective tissue, blood-vessels, lymphatics, nerves, and ganglia. The muscular fibres are of an irregularly cubical form, faintly striated transversely, from 1 / 500 to 1 / 350 inch in length by 1 / 1600 to 1 / 1000 . inch in breadth, destitute of sarcolemma, frequently having bands at the broad ends by which they anastomose, and showing an oval nucleus. A large mass of fibrous tissue and fibro-cartilage (which in some animals, as the ox, is bony) is found at the base of the heart, in the angle between the aortic and two auriculo-ventricular openings; from it processes pass in various directions, and form the bases of the fibrous or tendinous rings of the auriculo-ventricular and arterial openings, and to these many if hot all of the bands of muscular fibre are attached. These bands are arranged in layers. According to Pettigrew (1864), there are seven layers of fibres forming the wall of each ventricle,—three external, one central, and three internal,—and they are so arranged that the first or outer external layer is continuous with the seventh or inner internal layer, the second with the sixth, and the third with the fifth. Ludwig (1849) gives a simpler arrangement,— (1) an outer longitudinal layer extending from the base, where the fibres are attached to the tendinous structures around the orifices, and passing obliquely towards the apex to enter by a twist into the interior of the ventricle; (2) an inner longitudinal layer composed of the same fibres of the outer layer,— some of these becoming continuous with the papillary muscles (fig. 2) and others forming an irregular stratum of fibres, which terminate in the fibrous rings at the base of the ventricle (fig. 3); and (3) an intermediate or transverse layer, the thickest of the three, formed of fibres passing with less and less obliquity until they are transverse. These arrangements are shown in figs. 4 and 5, and they account for the following physiological phenomena. (1) The auricles contract independently of the ventricles. So long as the rhythmic movement is normal, the auricular contractions are equal in number to the ventricular; but, as the heart dies, there may be several beats of the auricle for one of the ventricle, and at last only the auricles contract. The auricular portion of the right auricle is the last to cease beating; hence it is termed the ultimum moriens. Sometimes also contractions of the vena cava and pulmonary veins may be noticed after the heart beats have ceased. (2) The contraction of the circular fibres around the orifices of the veins empties these vessels into the auricles; and no doubt these fibres have also a sphincter-like action during the contraction of the cavities, preventing the regurgitation of blood, and thus doing away with the necessity for valves at these orifices. (3) The double arrangement of fibres around the auricles produces, when the fibres contract, a uniform diminution of the auricular cavity. (4) The spiral arrangement of the fibres in the ventricular walls expels the blood with great force, as if it were propelled by wringing or twisting the walls of the cavity.

The valves of the heart are as follows (see Anatomy, vol. i. p. 900, fig. 89). (1) The tricuspid guards the right auriculo-ventricular opening, and consists of three flaps, formed of fibrous tissue (containing many elastic fibres) covered with endocardium. These flaps are continuous at their base, forming an annular membrane surrounding the auricular opening, and they are kept in position by the chordae tendineae, which are attached to their ventricular surfaces and free margins. (2) The bicuspid or mitral valve, at the left auriculo-ventricular orifice, consists of two pointed segments or cusps, having the same structure as those of the tricuspid valve. The auriculo-ventricular valves contain striated muscular fibres, radiating from the auricles into the segments of the valve. These probably shorten the valves towards their base and make a larger opening for the passage of the blood into the ventricles. A concentric layer of fibres, found near the base of the segments, has a sphincter-like action, approximating the base of the valves (Paladino). Some of the larger chordae tendineae contain striated muscle (Oehl), whilst a delicate muscular network exists in the valvulae Thebesii (guarding the openings of small veins from the substance of the heart into the right auricle) and in the Eustachian valve (a crescentic fold of membrane in front of the opening of the inferior vena cava) (Landois). The aortic and pulmonary openings are guarded by the sigmoid or semilunar valves, each of which consists of three semicircular flaps, each flap being attached by its convex border to the wall of the artery, whilst its free border projects into the interior of the vessel. The segments consist of fibrous tissue covered with endocardium. At the middle of the free border there is a fibro-cartilaginous thickening called the nodulus or corpus Arantii. From this nodulus numerous tendinous fibres radiate to the attached border of the valve, but along the margin of the valve the membrane is thin and destitute of such fibres. These thin parts are called the lunula. Opposite each semilunar flap there is a bulging of the wall of the vessel, the sinuses of Valsalva. In the aorta these are situated one anteriorly and two posteriorly (right and left). From the anterior arises the right coronary artery, and from the left posterior the left coronary artery,—these vessels being for the supply of blood to the substance of the heart (Quain).

According to Laennec, the size of the heart is about equal to the closed fist of the individual. Its mean weight is about 9 to 10 oz. John Reid’s tables give the average weight in the adult male as 11 oz. and in the female as 9 oz. The proportion of the weight of the heart to that of the body is from 1 to 150 to 1 to 170 (Quain). W. Miiller gives the ratio of heart weight to body weight in the child, and until the body weighs 88 lb, as ∙176 oz. to 2∙2 lb; when the body weight is from 110 to 200 lb the ratio is ∙141 oz. to 2∙2 lb; and when the weight of the body reaches 220 lb the ratio is as ∙123 oz. to 2∙2 lb. The volume of the heart, according to Beneke, is as follows :—new-born infant, 1∙34 cubic inches; 15 years of age, 9∙15 to 9∙76; at 20 years, 15∙25; up to the 50th year, 17∙08 cubic inches; after that there is a slight diminution. There is scarcely any difference between the capacities of the two ventricles, although in the ordinary modes of death the right is always found more capacious than the left, probably because it is distended with blood; the left ventricle after death is usually empty and more contracted. The wall of the left ventricle is much thicker than that of the right. The specific gravity of heart muscle is 1∙069. The thickness of the left ventricle in the middle is in man ∙44 inch and in woman ∙43; that of the right is ∙16 and ∙14 inch respectively. The circumference of the tricuspid orifice in man is 4∙62 inches and in woman 4∙33; of the mitral, 4∙13 and 3∙78 respectively. The circumference of the pulmonary artery is 2∙94 inches; of the aorta 2∙77; of the superior vena cava ∙702 to 1∙05 inch; of the inferior vena cava 1∙05 to 1∙4; and the diameter of the pulmonary veins, ∙53 to ∙62.

When the hand is applied to the side, a little to the left of the left nipple, and in the interval between the fifth and sixth ribs, a shock or impulse is felt. If the whole hand be placed flat over the region of the heart, one may notice the presence or absence of the heartbeat, also its situation and extent, and any alterations in its character. In some rare cases, where there is a congenital fissure of the sternum, the finger can be applied to various parts of the heart’s surface, with the integuments and pericardium intervening. This mode of examination may be termed palpation. Again, when the ear is applied, either directly, or indirectly by means of the stethoscope, over the position of the heart, sounds are heard the duration and rhythm of which are of physiological significance. This mode is known as auscultation. By percussing over the region of the heart the anatomical limits of the organ may be exactly defined, and information obtained as to its actual size, as to any alterations in the relation of the lungs to the heart, and as to the presence or absence of fluid in the pericardium. The direct registration of the movements of the heart has been accomplished by the aid of various recording instruments.

The movements of the heart consist of a series of contractions which succeed each other with a certain rhythm. The period of contraction is called the systole, and that of relaxation the diastole. The two auricles contract and relax synchronously, and these movements are followed by a simultaneous contraction and relaxation of the ventricles. Thus there is a systole and diastole of the auricles and a systole and diastole of the ventricles. But in each half of the heart the contractions and relaxations of the auricle and the contractions and relaxations of the ventricle are successive. Finally, there is a very short period in which the heart is entirely in diastole. The whole series of movements, from the commencement of one auricular systole to the commencement of the one immediately following, is known as the cardiac cycle or period of revolution of the heart. In fig. 6 the systole is represented by the curve above the horizontal lines and the diastole by the curve below them. The auricular changes are traced on the upper line au and those of the ventricle on the lower line vent. The length of the lines represents the total duration of a cardiac revolution. The diagram shows that the auricular systole occupies one-fifth of the total time of a revolution of the heart and the ventricular systole two-fifths, that the auricular systole immediately precedes the ventricular systole, that the commencement of the ventricular systole coincides with the commencement of the auricular diastole, and that during two-fifths of the total period both auricles and ventricles are in a state of diastole. There are thus three periods,—

(1) one of auricular systole, one-fifth; (2) one of ventricular systole, two-fifths; and (3) one of repose, two-fifths. The impulse of the apex against the wall of the chest, the moment of which is indicated by ×, occurs at the middle of the time occupied by the ventricular systole.

In 1861 Chauveau and Marey obtained a direct record of the movements of the heart of a horse, determined the duration of the events happening in the heart, and measured the endocardiac pressure by an instrument termed a cardiac sound. When the sound was introduced into the right auricle and right ventricle,—the animal being anaesthetized,—the tracings shown in fig. 7 were obtained. From this diagram we learn the following facts. (1) The auricular contraction is less sudden than the ventricular, as is indicated by the line ab being more oblique than the line c ' d'.

(2) The auricular contraction lasts only for a very short time, as the curve almost immediately begins to descend, whereas the ventricle remains contracted for a considerable time, and then slowly relaxes. (3) The time of the contraction of the auricle and that of its relaxation are about equal, but the time of the relaxation of the ventricle is nearly twice as long as that of its contraction; the movements of the auricle are thus uniform and wave-like, whilst those of the ventricle have more of a spasmodic character. (4) The auricular movement (ab, a'b', a"b", g, g', g") precedes the ventricular, and the latter coincides with the impulse of the apex against the wall of the chest, as is seen from the second vertical dotted line. (5) The contraction of the auricle, by forcing blood onwards, affects the pressure for an instant in the ventricle, as is indicated by the little elevation immediately before the ventricular contraction. (6) During the period of contraction of the ventricle there are oscillations of pressure affecting both the auricle and the ventricle; these are indicated by the little waves d, e,f, d', e',f, d", e", and f "; similar waves are seen at h , i , h', i', h", and i". The letters k, e, k', e', and k", e" represent a third set of waves.

With these facts in view, we may now describe the phenomena which happen in a complete cardiac revolution. Suppose the blood to be pouring from the venae cavae and the pulmonary veins into the two auricles. At that moment the auricles are passing into a state of complete diastole, and their cavity is increased by the funnel-shaped aperture at the auriculo-ventricular openings formed by the segments of the valves guarding these orifices. The distension of the auricles is due partly to the pressure in the venae cavae and pulmonary veins being less than in the interior of the auricles and partly to the aspirating action of the thorax during inspiration, sucking, as it were, the blood from the veins outside the chest to those inside the chest, and thus favouring the flow of blood to the heart. During this time both ventricles are filling with blood, the auriculo-ventricular orifices being open. When the distension of the auricles is complete (which happens before the distension of the ventricles, because the capacity of the auricles is much smaller than that of the ventricles), the auricular systole commences by the contraction and emptying of the auricular appendix towards the general cavity of the auricle, and by the mouths of the veins becoming narrowed by contraction of the circular fibres in their coats. These rhythmic movements are propagated quickly over the auricular walls, causing them to contract simultaneously towards the auriculo-ventricular orifices. The contracting wall forces the blood chiefly in the direction of least resistance, that is, into the ventricle, which at the same time is only partially full of blood, and is passing into a state of complete relaxation. The pressure in the veins, aided by their rhythmic contraction at the commencement of the auricular systole, is sufficient to prevent the blood from passing backwards, except to a very slight extent; but there is a momentary arrest of the flow in the large venous trunks. Thus the auricles act, not only as passive reservoirs for the blood in its passage from the veins to the auricles, but as rhythmic cavities tending to keep up a mean pressure in the veins, in diminishing by their extensibility the pressure which tends to increase during the ventricular systole, and in increasing the pressure by their contraction at a time when the venous pressure would diminish, that is, towards the close of the ventricular diastole. Both auricles and ventricles exercise, during their diastole, a certain aspirating or sucking action, like that seen during the relaxation of a compressed indiarubber bag; but this force is very feeble in the case of the heart.

The amount of blood discharged into the ventricles (already partially filled during the relaxation of the auricles) by the auricular systole is sufficient to fill their cavities, and consequently the ventricular systole immediately follows the contraction of the auricles. During the inflow of blood from auricles to ventricles the auriculo-ventricular valves are floated upwards into a more or less horizontal position, and the assumption of this position is further aided by the contraction of the longitudinal muscular fibres that pass from the auricles into the cusps of the valves. When the ventricular walls contract, the margins of the auriculo-ventricular valves are closely pressed together, and the cusps are kept from being folded backwards into the auricle by the simultaneous contraction of the musculi papillares pulling on the chordae tendineae which are affixed to the ventricular aspect of the valves. The close apposition of the cusps is also increased, even along their margins, by the arrangement that the chordae tendineae of one papillary muscle always pass to the adjoining edges of two cusps. Thus the valves, tricuspid on the right side and mitral on the left, are tightly closed and the blood cannot regurgitate into the auricles. The blood, thus compressed, can only pass into the pulmonary artery from the right ventricle and into the aorta from the left. The positive pressure in the ventricles is at its maximum at the beginning of their contraction; during the contraction it diminishes; and at the close of the systole (Marey), or in the diastole immediately thereafter (Goltz and Gaule), or even, according to Moens, shortly before the systole has reached its height, the pressure may even become negative. Moens “explains this aspiration as being due to the formation of an empty space in the ventricle caused by the energetic expulsion of the blood through the aorta and pulmonary artery” (Landois and Stirling). As the blood passes from the ventricles into the pulmonary artery and aorta, the segments of the sigmoid valves are forced open and stretched across the dilatations or sinuses behind each cusp, without being actually pressed against the walls of the vessels; and, as both the pulmonary artery and the aorta contained a certain amount of blood before, the pressure in these vessels is increased, and the walls of both yield to a considerable extent. As already stated, the ventricle continues in the contracted state for a brief space of time, and then it relaxes. Simultaneously with the commencement of relaxation, the auriculo-ventricular orifices open, thus permitting the passage of blood from the auricles; and at the same time the elastic walls of the aorta and pulmonary arteries recoil and force a portion of the blood backwards towards the cavities of the ventricles, in which, as they are passing into diastole, the pressure is much less than in the vessels. This blood, however, by filling the sinuses of Valsalva and the crescentic pouches of the sigmoid valves, closes these latter, and thus prevents any blood from passing into the ventricles. From the end of the ventricular contraction to the moment when the auricles are again full, all the cavities of the heart are in a condition of dilatation and the cavities are filling with blood. This is the period of the pause, during which the heart may be supposed to be in a state of rest.

When one watches an actively beating heart exposed in an anaes-thetized animal, the movements are so tumultuous and rapid that the eye cannot follow them so as to convey to the mind a correct conception of the rapid changes in form. Owing to this our notions of such changes have been derived chiefly from an inspection of the heart after death. Recent ingenious investigations by Ludwig and Hesse have shown that the post-mortem form is not the natural shape of the living heart either in diastole or in systole, but such as is shown, for example, in fig. 8.

The apex beat or shock of the heart is synchronous with the systole, and is caused normally by the apex of the ventricle pressing more firmly against the chest wall, from which it is separated when the heart is at rest by the thin margin of the lung. At the time of ventricular systole, as already seen, the heart, instead of being an oblique cone having an elliptical base, as in rest, becomes more like a regular cone, having a circular base. When contraction occurs, the apex is carried from below and behind, upwards and forwards, and. is forced into the intercostal space, and at the same time the ventricular portion twists on its long axis from left to right, so as to expose partially the left ventricle. It is the twisting motion that gives the shock or impulse, and it is caused chiefly by the contraction of the oblique fibres in the ventricles which lift up the apex; it is also assisted by the slightly spiral arrangement of the aorta and pulmonary artery. Some have supposed that the movement is partly due to the recoil of the ventricles after discharging their blood (like that of an exploded gun), causing the apex to go in the opposite direction, downwards and outwards; others have held that the discharge of blood into the pulmonary artery and aorta causes an elongation of these vessels, whereby the apex is pushed downwards and forwards. Both of these mechanisms, however, must have only a slight effect, as the cardiac impulse occurs even when from haemorrhage the pulsating heart is practically empty.

To obtain a tracing of the apex beat an instrument termed the cardiograph is employed, various forms of which are figured in Landois and Stirling’s Human Physiology, vol. i. p. 89 sq. Figs.

9 and 10 are examples of tracings obtained by this instrument. From the latter figure we learn the subjoined information. The time of the pause and the contraction of the auricle are represented by ab, and it is evident that the latter phenomenon causes the apex of the heart to move towards the intercostal space. The portion bc corresponds to the contraction of the ventricles and is synchronous with the first sound. The curve then rapidly falls as the ventricles relax, and during the descent there are two elevations, d and e, synchronous with the second sound. As already stated, when the ventricles relax, the blood in the aorta and pulmonary artery, driven backwards by the elastic recoil of the walls of these vessels, closes the semilunar valves.

This shock is propagated to the apex of the ventricles and thus causes a vibration of the intercostal space. The elevation d is synchronous with the closure of the aortic valves and e with that of the pulmonary valves; it is also apparent that these valves are not closed at the same moment, but are separated in time by ∙05 to ∙09 of a second,—an effect due, as already explained, to the greater blood pressure in the aorta than in the pulmonary artery. Finally, ef corresponds to the remaining part of the ventricular diastole.

Much discussion has taken place as to whether the contraction of the heart is to be regarded as a simple contraction, like the “twitch” of a muscle obtained by a single stimulation, or as a tetanic contraction, like cramp, such as is caused by the application of a number of stimuli in rapid succession. It is true that many of the phenomena of a cardiac contraction resemble those of a skeletal muscle: thus, fatigue diminishes the amplitude and increases the duration of the contraction; and the effects of changes of temperature are similar. The period of latent stimulation of a cardiac muscle (one-third of a second) is much longer than that of skeletal muscle (one-hundredth of a second). The systolic contraction, as regards duration, is more like a tetanic spasm than a twitch, being from eight to ten times longer. The electrical phenomena, on the other hand, resemble those of a twitch more than those of tetanus. Thus, when the heart is examined with a sensitive galvanometer, and with the aid of the appliances described under Physiology (vol. xix. p. 24 sq.), there is a “negative variation” with each beat. The fact appears to be that, just as the heart muscle shows histological characters intermediate between voluntary striated muscle and involuntary non-striated muscle, so it likewise shows physiological properties partaking of both.

The time occupied by cardiac movements has been measured by various observers by a study of tracings obtained from the impulse of the apex of the heart against the wall of the chest, as recorded by the cardiograph. If the velocity of the surface on which the tracing is obtained be known, and if a correct interpretation is given of the causes of the various parts of the curve, it is not difficult to determine approximately the time occupied by the phases of a cardiac revolution. Rollett gives the following results in fractions of a second as determined by Landois (Hermann, Handb. d. Physiol., vol. iv. p. 157). [table]

In the adult man cardiac pulsations occur at the rate of 65 to 75 per minute. There is a certain relation between the amount of blood in the circulation and the frequency of heart-beats. Thus, in the animal series, as the beats of the heart increase in frequency the quantity of blood which passes per minute in one kilogramme (2∙2 lb) of body weight also increases, as is shown in the following table by Vierordt :— [table]

It has been determined, both by direct measurement and by calculation based on the velocity of the blood in the aorta and the transverse section of the orifice of that vessel, that from a heart of average size each left ventricular systole ejects about 180 grammes (6∙35 oz.). This is the figure usually given, but it must be regarded merely as approximative. The amount may vary even in the same individual according to the state of vigour of the muscular walls of the organ.

When the ear is applied over the cardiac region of the chest of a healthy man two sounds are heard, the one with greatest intensity over the apex and the other over the base of the heart. The dull long sound heard over the apex has received several names, such as the first, the long, the inferior, and the systolic sound, whilst that over the base,—clearer, sharper, shorter, higher,—has been called the second, the short, the superior, the diastolic sound. Suppose the heart sounds to be expressed by the syllables lupp dupp ; then the accent is on lupp (the first sound) when the stethoscope is over the apex—thus, lúpp dupp, lúpp dupp—and on dupp (the second sound) when over the base—thus, lupp dúpp, lupp dúpp. There is a pause between the second sound and the next succeeding first sound, and a much shorter pause (almost inappreciable) between the first and second sounds: thus—

At apex—lúpp dupp (pause), lúpp dupp (pause), lúpp dupp.

At base—lupp dúpp (pause), lupp dúpp (pause), lupp dupp.

These relations are well seen in fig. 11. Dr Walshe states that, if the cardiac cycle be divided into tenths, the first sound will last four-tenths, the short pause one-tenth, the second sound two-tenths, and the long pause three-tenths. There has been considerable difference of opinion as to the cause of the first sound. Some have supposed it to be due to vibrations of the auriculo-ventricular valves; others believe that it is muscular, and due to the contraction of the ventricles; not a few have attributed it to movements of the blood through the aortic and pulmonary orifices; whilst yet others have thought that it might be the result of a fusion of these effects. It is certainly not due to the shock of the heart against the chest wall, as it has been heard after removal of the heart from the chest. The most likely view is that it is a muscular sound, varying in quality from the ordinary sound of a contracting muscle in accordance with the peculiar arrangement of the cardiac fibres, and that this sound is modified by the vibrations of the tense auriculo-ventricular valves. The fact that the sound has been heard from an excised heart still pulsating but empty of blood strongly supports this view; and there is further the pathological evidence that in cases where the muscular walls have been much weakened by fatty changes (as in the advanced stages of typhus, fatty degeneration, &c. ) the first sound may disappear. No doubt exists as to the cause of the second sound: it is produced by the sudden sharp closure of the sigmoid valves. As already mentioned, the aortic and pulmonary valves do not close absolutely simultaneously.

For practical purposes it is important to bear in mind what is happening in the heart whilst one listens to its sounds. With the first sound we have (1) contraction of the ventricles, (2) closure of the auriculo-ventricular valves, (3) rushing of the blood into the aortic and pulmonary artery, (4) impulse of the apex against the chest, and (5) filling of the auricles. With the second sound we have (1) closure of the semilunar valves from the elastic recoil of the aorta and pulmonary artery, (2) relaxation of the ventricular walls, (3) opening of the auriculo-ventricular valves so as to allow the passage of blood from auricle to ventricle, and (4) diminished pressure of apex against chest wall. With the long pause there are (1) gradual refilling of the ventricle from the auricle and (2) contraction of the auricle so as to entirely fill the ventricle. The sound of the tricuspid valve is loudest at the junction of the lower right costal cartilage with the sternum, of the mitral at the apex beat, of the semilunar valves at the aortic orifice in the direction of the aorta, where it is nearest to the surface, at the second right costal cartilage, and of the valves at the pulmonary orifice over the third left costal cartilage, to the left and external to the margin of the sternum.

For an account of the mechanical work performed by the heart, see Nutrition, vol. xvii. pp. 685-686.

The heart is directly nourished by the blood flowing through its cavities in some of the lower Vertebrates, as the frog; but in the hearts of larger animals, in which nutritional changes must be actively carried on, there is a special arrangement of vessels or cardiac circulation. The coronary arteries originate at the aortic orifice in the region of the sinus of Valsalva, rather above the upper border of the semilunar valves, so that when the ventricle contracts the mouths of these arteries are not covered by the segments of the valves. The branches of the coronary arteries, after dividing and again dividing, penetrate the muscular substance and end in a rich plexus of capillaries, which carry arterial blood to the structure of the heart. From these the radicles of the cardiac veins originate, and these veins carry the blood, now rendered venous, into the right auricle by the larger anterior cardiac veins and by numerous small veins constituting the foramina of Thebesius or the venae minimae cordis. The coronary vein is dilated before entering the auricle, forming the coronary sinus, and at the junction of the vein with the dilated portion there is a valve consisting of one or two segments. Other veins enter the coronary sinus, each having a valve. These valves serve two purposes: (1) they interrupt the flow of blood during the contraction of the right auricle, preventing regurgitation and venous congestion of the wall of the heart, and (2), as the valves open towards the right auricle, they prevent the backward flow of blood during contraction of the ventricles and favour its onward flow, and thus the stream of blood is accelerated, as in the veins of a contracting muscle. The blood is sent through the cardiac circulation by the systole of the ventricle, and not, as was advocated by Brücke, during its diastole. Heart disease in advanced life, when the coronary arteries are often thickened and their calibre much diminished by sclerosis, may be shown by attacks of palpitation, weakness of the heart, altered rhythm, breathlessness, congestions, pulmonary oedema, haemorrhage, and faintings,—all due to interference with the normal nutrition of the heart.

In an organ so active as the heart the lymphatic system is necessarily largely developed. These vessels, acting like drainage-tubes for carrying away waste products, are found in great numbers beneath both the pericardium and the endocardium, and throughout the muscular tissue. Amongst the muscular fibres there are numerous lacunae or spaces lined by endothelial cells, which are the origins of the lymphatics. The lymph is carried into lymphatic glands between the aorta and the trachea, and ultimately finds its way into the right innominate vein and the thoracic duct.

It has been known from early times that the heart will continue to beat after its removal from the body. This is more especially the case with the hearts of cold-blooded animals. The frog’s heart may continue to pulsate for two and a half days, whilst that of a rabbit will do so only for a period of from three to thirty minutes. The average duration of the beats of the warm-blooded heart is said to be eleven minutes. The right auricular appendix, which beats longest, has been observed to pulsate in the rabbit fifteen hours after death, in the mouse forty-six, and in the dog ninety-six hours. After the heart has ceased beating, it may again be caused to contract by direct stimulation or by heat. The injection of arterial blood into the coronary vessels will restore excitability in the Mammalian heart after it has ceased to beat (Ludwig).

If a wide glass tube filled with smoke be inserted into one nostril, while the other nostril and the mouth are closed, the smoke will be seen to move with each pulsation of the heart (Stirling). This phenomenon has been studied by Ceradini and Landois. It is explained by the fact that when the heart contracts it occupies less space in the chest, and consequently, if the glottis be open, air will be drawn into the lungs. The reverse will happen during the diastole.

The heart and lungs being contained in an air-tight cavity, the chest or thorax, it is evident that the increase and decrease in the size of the chest during inspiration and expiration must affect the amount of pressure on the outer surface of the heart, and consequently its movements. When an inspiration is made by the descent of the diaphragm and the elevation of the ribs, the lungs expand; there is then less pressure on the outer surface of the heart and the heart is in a state of distension in diastole. In consequence also of the removal of pressure during inspiration from the great veins entering the chest and reaching the right side of the heart, the flow of venous blood towards the heart is favoured. These effects are more marked if after a deep expiration the glottis be closed, so as to prevent air entering the lungs, and if then the chest be dilated by a powerful inspiratory effort (J. Müller). This causes a dilatation of the heart, and venous blood flows freely into the right side; this sends it on to the lungs, causing them to become engorged, whilst at the same time the dilated left side of the heart is unable to send out a sufficient amount of blood into the arterial system. The pulse in such conditions may disappear, and there is an intense feeling of distress. On the other hand, expiration increases the pressure on the outer surface of the heart and of the great veins; only a small amount of blood flows into the right side; the heart is contracted; the systole is small; and the pulse is reduced in volume. This condition is intensified in what is termed Valsalva’s experiment, in which after a deep inspiration the glottis is closed and a powerful expiratory effort is made. When this is done, the flow of venous blood into the heart is interrupted, the veins in the face and neck swell, and the blood is forced out of the compressed lungs into the left side of the heart, which throws it into the arterial circulation. The pulse and heart sounds disappear and there is the risk of syncope or fainting. Both these experiments, Müller’s and Valsalva’s, are dangerous and should not be often repeated. They are extreme conditions of the normal state of things, in which inspiration favours the flow of blood into the heart and the dilatation of the heart, whilst expiration has the opposite effect; and they also explain the mechanism by which air may be sucked into the veins from wounds in the neck or armpit. This is most likely to occur during inspiration, and when it does occur speedy death is the result.

In treating of the innervation of the heart we have to consider (1) the influence of the great nerves connecting the heart with the central nervous organs, or what may be termed the extrinsic nervous mechanism, and (2) the nervous arrangements in the heart itself, or the intrinsic nervous mechanism. (1) The extrinsic arrangements, consisting of the nerves given off by the cardiac plexuses derived partly from the cerebro-spinal and partly from the sympathetic system, have been investigated chiefly in the larger animals, such as the tortoise, rabbit, and dog, and the general results have been described under Physiology (vol. xix. p. 29 sq.). They may be briefly summarized as follows: (a ) there are fibres in the vagus nerve exercising a controlling or inhibitory action on the heart, and these fibres originate in the medulla oblongata; (β) the sympathetic nerve supplies accelerating fibres to the heart, and these fibres originate in the cerebro-spinal system. (2) The intrinsic arrangements have been investigated more especially in the heart of the frog, a view of which is given in figs. 12 and 13. It will be seen that the frog’s heart possesses two auricles, communicating by a foramen in the septum, and a single ventricle. The venous blood from the body is poured in the first instance, not into the right auricle, but into a cavity called the sinus venosus, which communicates with the right auricle. The left auricle receives the arterial blood from the lungs by the pulmonary veins. Both auricles empty into the common ventricle, which contains therefore a mixture of arterial and venous blood, and when the ventricle contracts some of this blood is again sent to the lungs, whilst the remainder passes into a dilatation at the commencement of the arterial system, called the bulbus arteriosus, and thence into the aorta.

After the heart of a decapitated frog has been removed from its body, and so from the influence of the great nervous centres, rhythmical movements may continue for some time independently of those centres. If the apex of the heart be then cut off, it will remain motionless, whilst the larger part will still beat rhythmically. Successive slices may be removed from the larger portion without affecting rhythmical contraction, until a section is made through the auriculo-ventricular groove, when the ventricular portion of the heart ceases to beat. If the motionless apex, or the separate portions rendered motionless by the above procedure, be mechanically irritated, a single contraction, not a series of rhythmic contractions, follows. When the ventricle is separated from the rest of the heart by a ligature, or by concision at the level of the auriculo-ventricular groove, the ventricle stops, but the auricles and the sinus go on beating. To continue the rhythmic movement of the ventricle, it is necessary to have attached to it a small portion of the auricular part of the heart, especially the lower margin of the septum. It would, therefore, appear that impulses pass from this auricular portion into the ventricular and cause the latter to pulsate. If the sinus venosus be separated from the auricles by incision or ligature, the veins and the sinus continue to beat, whilst the auricles and ventricles are arrested in diastole. Suppose another incision be made through the auriculo-ventricular groove, the ventricle frequently begins to beat, but the auricles remain in diastole. It is also observed in these circumstances that the ventricle beats more slowly than under normal conditions. Although the rhythmical contractions of the heart are influenced by the nervous arrangements, it cannot be said that ganglionic nerve cells and nerve fibres are a necessary part of the mechanism. It has been shown by Engelmann that, if the ventricle of a frog’s heart be cut into two or more strips in a zigzag manner, so that the parts still remain connected with each other by muscular tissue, the strips still beat in a regular progressive manner, provided one strip is caused to contract.

The Action of the BloodVessels.

It is evident that a general study of the flow of fluids through tubes ought to precede that of the flow of the blood through the complicated system of tubes constituting the arteries, capillaries, and veins. In this place, however, it is necessary to allude only to those facts in hydraulics which have a special bearing on the phenomena of the circulation (comp. Hydromechanics, vol. xii. pp. 440 sq. and 459 sq.). When a stream of water is transmitted intermittently by the strokes of a pump through a long elastic tube, formed, say, of india-rubber, the fluid does not issue from the other end in a series of jets, which would be the case if the tube were rigid, but it flows continuously, because during the pause between the successive strokes the outflow still continues. Consequently a continuous flow is kept up in elastic tubes when the time between two strokes is shorter than the duration of the outflow after the first stroke. If the finger be placed on any part of such a tube, and more especially near the pump, an expansion and relaxation will be felt with each stroke. Further, if the right fore-finger be placed over the tube near the pump, and the left fore-finger over a more distant portion, a stronger impulse will be felt with the right than with the left finger. Thus a wave is transmitted along the tube, diminishing in amplitude as the distance from the pump increases. We must distinguish between the transmission of this wave (an oscillatory movement or change of form in the column of fluid) and the transmission of the current, that is, the translation of a mass of fluid along the tube. In elastic tubes the current is much slower than the transmission of the wave. The progress of the wave of oscillation may be traced graphically by an apparatus devised by Marey. E. H. Weber gives the velocity of waves in elastic tubes at 36∙76 feet per second, and Donders states it at 36 to 42½ feet. Increase of pressure in the tube appears to lessen the velocity of the wave. The specific gravity of the liquid also affects the velocity: thus the wave is propagated four times more slowly in mercury than in water.

The blood-vessels consist, as already stated, of the arteries, the capillaries, and the veins. (a ) The ultimate or most minute capillaries have the simplest type of structure (fig. 14), consisting of tubes formed of a single layer of transparent, thin, nucleated, endothelial cells, joined at their margins. A perfectly fresh capillary does not show the edges of the cells, owing to the uniform refractive property of the wall of the tube. The nuclei show an internuclear plexus of fibrils. The cement substance uniting the cells is stained black by a ¼ per cent. solution of nitrate of silver. Here and there minute dots or slits may be seen, which have been supposed by some to be openings (stomata or stigmata). In the transparent parts of animals, such as the web of the frog’s foot, the mesentery and the lung of the frog, and the tail of a fish, the blood may be seen (fig. 15) flowing through the capillary network from the arteries into the veins. The current is rapid in the small arteries, less rapid in the veins, and slow in the capillaries. It is also fastest in the centre of the vessel and slowest near the wall. The colourless corpuscles of the blood may be seen to pass from the centre of the stream to the margins, to adhere to the inner surface of the blood-vessel, and occasionally to pass through the coats of the more minute vessels, appearing in the surrounding tissues as migratory cells. Capillaries form networks (fig. 15), which vary much in the size and closeness of the meshes, according to the degree of activity of the tissue elements.

(b ) An artery has three coats,—an inner or elastic, a middle or muscular, and an external or areolar (fig. 16). The inner coat is formed of two layers,—one of pavement epithelium, sometimes called endothelium, and the other composed of fine elastic fibres interlacing, or of a fine membrane perforated with holes of various sizes (fenestrated membrane of Henle). In some vessels there is a thin layer of connective tissue between the epithelium and the elastic layer. The middle coat is formed of a layer of non-striated muscular fibres circularly disposed around the vessel, mixed with numerous elastic fibres connected with the perforated membrane of the inner coat. The outer coat consists of connective tissue, mixed also with elastic fibres. In the aorta there is a considerable amount of sub-epithelial connective tissue (Schäfer), and the elastic coat attains great thickness and strength. As a general rule, the smaller arteries show a considerable development of the muscular coat, whilst in the larger it is the elastic coat that attains the preponderance. In many of the larger arteries there are longitudinal muscular fibres at the boundary of the middle and inner coats. Whilst the circular fibres, on contracting, must narrow the calibre of the artery, the longitudinal may tend to keep the vessel open. In the external coat of the larger arteries minute vessels, vasa vasorum, exist for the nourishment of the tissue elements of the arterial wall.

(c) The veins have similar coats to those of an artery, with differences in detail. The elastic layer is less developed in the internal coat; the middle coat is much thinner and has less elastic tissue, but more connective tissue. Many veins have semilunar folds of the internal coat strengthened with fibrous tissue, forming valves. In some veins (iliac, femoral, umbilical) longitudinal muscular fibres are found in the inner part of the middle coat; in the inferior vena cava, hepatic veins, and portal veins these longitudinal fibres are external to the circular coat; in the superior vena cava and upper part of the inferior vena cava the circular coat is wanting; and the veins of the pia mater, brain and spinal cord, retina, bones, and the venous sinuses of the dura mater and placenta have no muscular tissue (Schäfer). Valves exist in the larger veins only, especially in those of the limbs; they are not found in the veins of the viscera, of the cranium and vertebral canal, or of the bones, nor in the umbilical vein.

(d) The arterioles and venules are the small vessels, simpler in structure than the larger above described, but containing the same elements. In the smallest veins the elastic layer has disappeared, and the muscular layer is also very thin. Sometimes the muscular layer is represented only by a single layer of contractile cells, and in such minute vessels the outer coat and elastic layer have also disappeared, so that the vessel is merely a tube composed of pavement cells with a few elongated fusiform muscular cells twisted around it. Even in the smallest vessels the following differences may be observed between arterioles and venules: “The veins are larger than the corresponding arteries; they branch at less acute angles; their muscular cells are fewer, and their epithelium cells less elongated; the elastic layer of the inner coat is always less marked, and sooner disappears” (Schäfer).

(c) The cavernous spaces, as existing in erectile tissues (corpus cavernosum of the penis), consist of the anastomosis of large veins of unequal calibre. The walls and partitions have numerous perforations; threads of delicate tissue, covered with epithelium, pass through the cavities; and the walls are strengthened by connective tissue. Similar structures connected with arteries form the carotid gland of the frog and the coccygeal gland of man.

The physical properties of blood-vessels are cohesion and elasticity. The cohesion is great and the elasticity is small and perfect. The walls of blood-vessels have the property of contractility, by which alterations take place in the calibre of the vessel, and consequently in the amount of blood supplied to a part.

Arterial Circulation.— The arterial walls are both muscular and elastic, the muscular coat predominating in the smaller, whilst the elastic coat is strong in the greater arteries. The chief function of the elasticity of the greater vessels is to transmute the unequal movement of the blood in the large arteries, caused by the inter mittent action of the ventricle, into a uniform flow in the capillaries. Thus, when the ventricle contracts, it propels a certain amount of blood into the elastic aorta, which expands in all directions. On the commencement of the diastole of the ventricle the vis a tergo is removed; the aorta owing to its elasticity recoils, so as to close, on the one hand, the semilunar valves and, on the other, to force part of its contents into the vessels farther onwards. These, in turn, as they already contain a quantity of blood, expand, recover by an elastic recoil, and transmit the movements with diminished intensity. Thus the blood is driven along the vessels by the action (1) of the ventricular systole, and (2) of the elastic recoil of the walls of the vessels occurring during the intervals between the ventricular systole (see p. 104 below). By these actions a series of movements, consisting of expansions and contractions, gradually diminishing in amplitude, pass along the arterial system from the greater to the smaller vessels, the latter becoming, as already pointed out, less and less elastic. These expansions and relaxations of the arterial wall, passing along like a wave, constitute the pulse. The pulse therefore represents merely the transmission of an undulating movement of the blood, not its progression in the vessels. The undulations of the pulse travel at the rate of 354 ⅓ inches per second, about 30 times faster than tho movement of the blood, which in the carotid artery of the horse has been estimated to travel 11∙8 inches per second.

The pulse can be registered graphically by means of a Sphygmograph (q.v. ). Vierordt constructed the first sphygmograph in 1855, substituting for a column of fluid a lever placed on the pulse, which communicated with a system of levers and thus amplified the movement. Of those subsequently devised the best form is that of Marey, invented in 1861. It consists essentially of a long lever, which is moved near the fulcrum by a screw acting on a small horizontal wheel, from whose axis there projects a long, light, wooden lever. The point of the screw rests on a flat disk of steel or ivory, at the end of an elastic spring, which presses the ivory disk or pad on the artery. The lever inscribes the movements on a blackened surface, usually a strip of paper smoked in the flame of a lamp burning turpentine, carried in front of the point of the lever by clock-work. In the instrument as modified by Mahomed, Byrom Bramwell, and others there is an arrangement for adjusting the amount of pressure made on the artery by the ivory pad, so that tracings may be taken at different times from the same artery with different or with the same pressures. The tracings are “fixed” by passing them through shellac or photographic varnish.

The fol lowing changes take place in an artery when it pulsates: —(1) it dilates and at the same time lengthens to a small extent; (2) the pressure of the blood increases in the artery, and a feeling of hardness and resistance is experienced when the artery is compressed with the finger. These facts are illustrated in the sphygmo-graphic curve shown diagrammatically in fig. 17. The ascending line ab (line of ascent, up-stroke, or percussion stroke) corresponds to the distension of the artery produced by the systole of the left ventricle, and the descending line bcd to its elastic recoil; the length of the line ad represents the total duration of the movement, which is divided into two portions by the perpendicular line be. The distance ae measures the duration of the distension of the artery and ed the time of its elastic recoil. In a continuous tracing the durations of the individual pulsations are equal, and in inverse ratio to the number of pulsations in a unit of time. In a normal pulse the distension and the elastic recoil of the vessel succeed each other without interruption, so that there is no period of repose in the artery. When, however, the pressure of blood in the artery falls below a certain point, these characters disappear or are modified. Fig. 17 shows that the duration of the distension of the artery is only about one-third of that of its contraction. The rapidity and slowness of the pulse depend on the ratio of these periods. The pulse is quick when the duration of the arterial distension diminishes, and slow when it increases. The line ab becomes less oblique and more nearly vertical, in proportion as the time of the distension is short, quick, and nearly instantaneous. The rapidity of the pulse is increased by quick action of the heart, considerable power of yielding in the arterial Avails, easy afflux of blood owing to dilatation of smaller vessels, and nearness to the heart. The term quickness has reference to a single pulse-beat, and frequency to the number of beats in a given time, say, one minute. The line bcd is always more oblique than ab, and in careful tracings it presents several elevations or notches (see fig. 18). If we refer the different portions of the curve to their origin the result is as follows:—(1) the up-stroke corresponds to the systole of the left ventricle, opening the aortic valves, pouring the blood into the arteries, and distending them; (2) the downstroke represents the time during which the blood is flowing out of the arteries at their periphery into the capillaries; (3) the larger wave in the descent, i.e., the dicrotic, recoil, or aortic systolic wave, represents the time of the closure of the aortic valves; (4) the predicrotic, first tidal, or second ventricular systolic wave occurs after the first systolic wave and during the ventricular contraction (Byrom Bramwell). In many pulse-tracings there are still smaller secondary waves, due to elastic vibrations of the wall of the vessel. The three factors causing an arterial pulsation are (1) the more or less energetic contraction of the ventricle, (2) the quantity and pressure of the blood, and (3) the elastic and contractile properties of the arterial wall. If these factors be in any way modified there will be a corresponding modification in the physical characters of the pulse. The character of a pulse-tracing is affected by the amount of pressure applied to the artery. With a light pressure the dicrotic wave is relatively less; with a moderate pressure (3½ to 7 oz.) it is well marked, whilst the curve is lower; and with greater pressure it is again reduced. With 7¾ to 10½ oz. pressure small secondary waves appear before the dicrotic.

The normal pulse-rate in man is about 72 per minute, in woman about 80 per minute; but in some individuals a state of health is consistent with a pulse-rate as rapid as 100 or as slow as 50 beats per minute. The pulse-rate is influenced by the undermentioned factors. (1) Age : a newly-born child, 130 to 140 beats per minute; 1 year, 120 to 130; 2 years, 105; 3 years, 100; 4 years, 97; 5 years, 94 to 90; 10 years, about 90; 10 to 15 years, 78; 15 to 50 years, 70; 60 years, 74; 80 years, 79; 80 to 90 years, over 80. (2) Length of body : Czarnecki, Volkmann, and Rameaux have shown that as the height increases the pulse slows. (3) Bodily states: active muscular exercise, increased blood-pressure, active digestion, pain, nervous excitement, extreme debility quicken the pulse. (4) Temperature : increase of temperature quickens the pulse. An increase of 1° above 98° Fahr. is associated with an increase of 10 beats per minute: thus, at 98° Fahr. the pulse-rate will be 60 per minute; at 99°, 70; at 100°, 80; at 101°, 90; at 102°, 100; at 103°, 110; at 104°, 120; at 105°, 130; and at 106°, 140 (Aitken). (5) Posture: the pulse is more frequent when one stands than when one sits, and still slower when one lies down. (6) Sensory impressions : music is said by Dogiel to quicken the pulse. (7) Pressure : increased barometric pressure slows the pulse. (8) Diurnal rhythm : 3 to 6 A.Μ., 61 beats; 8 to 11.30 A.Μ., 74; towards 2 p.m., a decrease; towards 3 (at dinner-time) another rise, which goes on until 6 to 8 p.M., when it may be 70; towards midnight, 54; a rise again towards 2 A. μ., when it soon falls again, and afterwards rises, as before, towards 3 A. Μ. (Landois and Stirling).

Colin gives the following pulse-rates in various animals elephant, 25 to 28 heats per minute; camel, 28 to 32; giraffe, 66; horse, 36 to 40; ox, 45 to 50; tapir, 44; ass, 46 to 50; pig, 70 to 80; lion, 40; lioness, 68; tiger, 74; sheep, 70 to 80; goat, 70 to 80; leopard, 60; wolf (female), 96; hyaena, 55; dog, 90 to 100; cat, 120 to 140; rabbit, 120 to 150; mouse, 120; goose, 110; pigeon, 136; hen, 140; snake, 24; carp, 20; frog, 80; salamander, 77.

A pulse is said to be strong or weak according to the weight it is able to raise. The strength is usually estimated by pressing the finger on the artery until the pulse-beat beyond the point of pressure disappears. The pulse is said to be hard or soft according to the degree of resistance experienced. In feeling the pulse it is important to notice whether the tension is great during the distension of the vessel, or whether it is hard during the intervals between the pulse-beats as well as during the beats themselves. On the other hand, it may be soft in these intervals in consequence of the semilunar valves at the aorta not closing perfectly (aortic incompetence), thus allowing the blood partially to flow back into the ventricle. This softness and the feeling of sudden collapse of the arterial wall are the pulse characteristics of unfilled arteries. A pulse may be large in volume, as where a large amount of blood is thrown into the aorta, owing to hypertrophy of the left ventricle, or it may be small and thready when a small quantity of blood passes into the aorta, either owing to a diminished total amount of blood, or from constriction of the aortic orifice (aortic stenosis), or from disease of the mitral valve allowing the blood to regurgitate into the left auricle, or when the ventricle contracts feebly.

The pulse becomes later and later in time as we recede from the heart. Czermak estimated the delay as follows:—carotid pulse, after the cardiac beat, ∙087 second; radial, ∙159 second; posterior tibial, ∙193 second. By placing delicate tambours or electromagnetic sphygmographs at different points of the circulation and recording the movements on a rapidly moving surface, E. H. Weber found the velocity of the pulse-wave to be 30∙31 feet per second; Garrod found it to be from 29∙52 to 35∙43 feet per second; Crashey determined it at 27∙89 feet per second; and Moens at 27∙23. In the arteries of the upper limb it is stated to be 30∙84 and in those of the lower limb 31∙82 feet per second. The wave-length is obtained “by multiplying the duration of the inflow of blood into the aorta =∙08 to ∙09 second by the velocity of the pulse-wave.” This would give the wave-length at 2∙46 feet.

As already pointed out, inspiration favours the flow of blood into the veins and retards the flow in the arteries, whilst expiration has the reverse effect. The tension of the arteries during inspiration is therefore less than in expiration, and this affects the form of the pulse-curve, as is seen in fig. 19. (1) “The greater distension of the arteries during expiration causes all the parts of the curve occurring during this phase to be higher; (2) the line of ascent is heightened during expiration, because the expiratory thoracic movement helps to increase the force of the expiratory wave; (3) owing to increase of the pressure the dicrotic wave must be less during expiration; and (4) for the same reason the elastic elevations (secondary waves) are more distinct and occur higher in the curve near its apex” (Landois and Stirling, op. cit.). See also p. 102 above.

Non-striated muscle, as has been already stated, exists to a considerable amount in the walls of the smaller arteries, and the calibre of these vessels may consequently be changed by the activity of the contractile coat. The contractility of vessels may appear under two forms :—(1) as rhythmical contractions, such as have been seen in the vessels of a rabbit’s ear or in a bat’s wing, which are independent both of the pulse and of respiratory movements; and (2) as persistent contractions, under the influence of the nervous system, which play an important part in the distribution of the blood. The amount of contraction of an artery will affect the pressure of the blood in its interior: it will accelerate or retard the rapidity of the blood current; and it will regulate the supply of blood to the capillary area to which the vessel is distributed. By such arrangements, also, the distribution of blood to various organs is regulated, thus establishing what has been termed a balance of local circulations. For example, if the vessels in one organ remain permanently contracted, whilst those in a neighbouring organ are dilated, more blood will pass to the latter than to the former, and some end of physiological importance may be served. Thus physiological correlations may be established between the cerebral and thyroid circulations, the gastro-hepatic and the splenic circulations, and the distribution of blood in the lower extremities as related to the abdominal organs.

If a stethoscope be placed over a large artery, a murmur, sound, or bruit will be heard, caused by the blood rushing through the vessel narrowed by the pressure of the instrument. The fluid escapes into a wider portion of the vessel beyond the point of pressure, and the sound is caused by the particles of fluid there being thrown into rapid vibration, not by vibrations of the wall of the vessel. Such sounds are favoured by a certain degree of elasticity in the walls of the vessel, by diminished peripheral resistance allowing the blood to flow away freely, and by a considerable difference of the pressure in the narrow and wide parts of the tube. They are always heard over an aneurism, when the arterial tube is dilated, and when pressure is applied to a large vessel. The placental souffle or bruit heard during pregnancy is a sound of this kind, arising from pressure on the widely dilated uterine arteries. In cases of insufficient aortic valves a double blowing murmur may be heard, the first being due to the rush of blood into the vessel caused by the ventricular contraction, and the second by the flowing back of the blood into the heart during diastole. Comp. p. 106 below.

Capillary Circulation.— The circulation in the capillaries may be readily studied by placing under the microscope any transparent membrane containing vessels, such as the web of a frog’s foot, the mesentery, lung, or tongue of a frog, the tail of a fish or a tadpole, the wing of a bat, the third eyelid of the pigeon or fowl, the liver of a frog or a newt, the mucous membrane of the inner surface of the human lip, or the conjunctiva of the eyeballs and eyelids. Under favourable conditions the following phenomena may clearly be noticed. (1) The diameter of the finest capillaries is such as to permit the passage of corpuscles in single file only, and it may vary from 1 / 5000 to 1 / 12,500 of an inch. (2) The average length is about 1 / 50 of an inch. (3) The number varies according to the degree of activity of the tissue, being numerous where nutritive processes are active, as in the liver and muscles. (4) They form networks or anastomoses, the form and arrangement of which are determined by the tissue elements. (5) In the smaller arterioles and venules, and in the capillaries, the current is continuous and there is no pulse. Owing to the elasticity of the larger vessels the intermittent movement of the blood caused by each ventricular contraction is in the capillaries transformed into a continuous flow. (6) In some of the larger vessels the current is more rapid than in others of equal calibre: that is to say, it is more rapid in small arteries than in small veins. (7) The current appears to have a uniform velocity in all ultimate capillaries of the same size. (8) Sometimes a slight acceleration of the rapidity, even in the smallest vessels, may be observed to follow each cardiac beat. (9) In a vessel larger than an ultimate capillary, so large as to permit the passage of several coloured corpuscles abreast, these may be seen travelling with great apparent velocity in the centre of the stream, whilst the colourless corpuscles move more slowly and with a rolling motion next the walls of the tube, in a layer of plasma called Poiseuille’s space. The coloured corpuscles also remain separate from each other, and do not exhibit any tendency to adhere together or stick to the walls of the vessels, whereas the colourless corpuscles do both, more especially after the membrane has been exposed for some time to the air, so as to excite the early stages of inflammation. Prof. D. J. Hamilton has shown that the nearer a suspended body approaches the specific gravity of the liquid in which it is immersed the more it tends to keep in the centre of the stream, and he states that the reason why the coloured corpuscles keep the centre and the colourless the sides of the stream is that the specific gravity of the former is the same or slightly greater than the blood plasm, whilst that of the colourless corpuscles is less. (10) If the calibre of an ultimate capillary be marked at the beginning of an observation, and again some time afterwards, it will frequently be noticed that it has become narrower or wider, indicating that contractility is one of the properties of capillaries. (11) The velocity is greater in the pulmonary than in the systemic capillaries. (12) The phenomenon known as diapedesis, or migration of the white blood corpuscles, first described by Waller in 1846, is readily seen in the mesentery of the frog after inflammation has been excited by exposure to the air for one or two hours (see fig. 20). It consists of the adhesion to the wall of the vessel of the colourless corpuscles and their protrusion through the wall into the surrounding tissues. Hering is of opinion that it is due partly to the filtration of the colloidal matter of the cell under blood-pressure. Diapedesis is of importance as constituting a part of the inflammatory process. The colourless cells become pus corpuscles (Cohenheim); see Pathology, vol. xviii. p. 365. (13) If a vascular membrane be gently irritated whilst under the microscope, the capillaries become first slightly narrowed and then dilated, crowded with corpuscles, whilst the blood - stream becomes slower. By and by the stream oscillates and then altogether stops. This constitutes stastis, a part of the inflammatory process, and is followed by exudation of the plasma of the blood, along with colourless corpuscles, and more rarely coloured corpuscles.

The most important vital property of capillaries is, as already mentioned, contractility, by which their calibre may be modified. The protoplasm forming their walls contracts when stimulated. Some investigators have supposed the nuclei to be active agents in contraction; but more probably the cell substance is the seat of change. Oxygen causes the nuclei to swell, whilst carbonic acid has the opposite effect. Roy and Graham Brown attach much importance to the active contractility of the capillaries as regulating the distribution of blood, now contracting, now relaxing, according to the needs of the tissues in their vicinity. Elasticity is also a characteristic of the capillary walls.

The arrangement of the capillaries in an organ or tissue is adapted to its functional activity. Where there is great functional activity there is a rich plexus of capillaries, and in the converse case the converse is also true. Contrast, for example, the capillary supply in cartilage with that of muscle, or that of the grey matter of the nerve centres with that of the white matter (see Physiology, vol. xix. p. 23 sq.). But, in addition, the distribution of capillaries always corresponds to the intimate structural arrangements of the tissue or organ. So precisely is this the case that a good histologist is able to identify the organ from an injected preparation showing the vessels, although none of the ultimate histological elements of the organ or tissue are to be seen. In muscle, for example, the capillaries exist in the form of elongated meshes; in connective tissue, such as is found beneath the skin, in an irregular network; in the papillae of the skin, in loops; and to form the glomeruli of the kidney in close reticulations (see Nutrition, vol. xvii. p. 673, fig. 5).

The movement in the capillaries is due to the force of the heart, as modified by the vessels (vis a tergo). Some have supposed that it is supplemented by an attractive influence exerted by the tissues (vis a fronte) ; and the statement is supported by the observation that, when there is an increased demand for blood owing to active nutritional changes, there is an increase in the amount of blood flowing to the part, such as occurs, for example, in the mammary gland during lactation, and in the growth of the stag’s horn. Such an attractive influence on the part of the tissues is quite conceivable as a force assisting in the inward flow of blood, acting along with capillarity; but its amount is infinitesimally small in comparison with the force exerted by the heart. The force of the heart is sufficient to drive the blood through the capillaries into the veins.

When capillaries are examined in a transparent membrane of a living animal no pulse-like movement is visible. Owing to the elasticity of the vessels the pulse-wave has been almost, if not quite, extinguished, and what might have remained of it is destroyed by the great resistance offered by the numerous capillaries. If these and the arterioles be widely dilated, a pulse may appear in the veins, as occurs when the vaso-dilator fibres of the chorda tympani nerve are stimulated, causing a pulse-like movement in the veins of the sub-maxillary gland (see Physiology, vol. xix. p. 30). By increasing the extra-vascular pressure pulsations may occur in the capillaries (Roy and Graham Brown). The well-known throbbing in the finger when constricted by an india-rubber band and the throbbing of inflammatory swellings are examples of pulsation in capillaries.

Venous Circulation.— The walls of the veins are thinner, less elastic, and more distensible than the walls of the arteries. They contain both elastic and contractile tissue, though to a smaller extent than the arteries. Numerous anastomoses exist between veins and even between superficial and deep veins, so that if the flow of blood be obstructed in one direction it readily finds a passage in another. The circulation in the veins depends (1) on inequality of blood-pressure, the pressure being much less in the veins than in the arteries; (2) on muscular action compressing the veins, and thus, in consequence of the valves found in many veins opening towards the heart, forcing on the blood in the direction of that organ; (3) on the movements of respiration,—inspiration, as already seen, favouring the flow of blood in the great veins towards the heart; and (4) on the suction-like action of the right auricle, and in the case of the lungs that of the left auricle, drawing the blood towards the heart. During venesection, muscular action increases the flow of blood from the divided vein; hence the use of the barber’s pole, which was grasped by the patient during bleeding by the barber-surgeon of old. The flow of blood in veins is continuous, or nearly so; when, therefore, a vein is cut, it does not “spurt” as an artery does, but it “wells out” in a stream.

There is normally no pulse in veins; but sometimes a pulse may be observed in the veins of the neck, isochronous with the auricular systole, when there is an obstruction to the passage of blood from the right auricle into the right ventricle. Pulse-tracings (fig. 21) taken in these circumstances are very similar to those of the cardiac impulse. In this tracing the part ab represents the right auricular contraction. During the systole of the right ventricle the tricuspid valve closes, and, if it be insufficient,—that is, if it does not close properly,—a positive wave is transmitted along the superior vena cava to the jugular (bc in the pulse-tracing). The closure of the pulmonary is indicated at e. During the diastole of the right auricle and ventricle the blood flows to the heart and the curve descends, f. It has also been pointed out by Friedreich that a pulse in the jugular vein does not necessarily mean insufficiency of the tricuspid valve but a weakened condition of the valve in the jugular vein itself, as the pulse will not be propagated into the jugular, even in cases of insufficiency of the tricuspid valve, if the jugular valve be perfect. If there is great obstruction at the mitral orifice, a venous pulse may also be observed, which is associated with engorgement of the right auricle. Sometimes a pulse in the veins occurs when there is such rigidity from atheroma in the walls of the great vessels as to destroy the elastic influence of these parts, and at the same time such a degree of dilatation of the arterioles and capillaries as to admit of the onward propulsion of the movement caused by the heart’s contraction. Lastly, a pulse may occur when the blood-pressure rises and falls suddenly, as in insufficiency of the aortic valves, and when the arterioles are much dilated. Towards the close of life, when the heart is feeble and effusion may be taking place into the pericardium, a venous pulse may be observed.

If a stethoscope be placed at the root of the neck above the collar bones, and on the right side in particular, a whistling, rushing, or blowing sound will be heard. This is the bruit de diable, familiar to physicians. If heard without pressure being made by the stethoscope it is abnormal, as it occurs in conditions of anaemia from almost any cause; but it may be heard in a healthy person when pressure is applied and when the head is turned to the opposite side. It is held to be due to the vibration of the blood in rushing from the contracted portion of the common jugular vein into the more dilated part of this vessel. During the auricular diastole and during inspiration it is more marked, as the blood then flows more rapidly in the veins towards the heart.

Phenomena of General Circulation.

Having described the structure and functions of the organs concerned in the circulation,—namely, heart, arteries, capillaries, and veins,—we are in a position to consider the phenomena of the circulation as a whole. Consider the organs of the circulation as a closed system of tubes, over-filled with blood; when the tubes are in a state of rest, it is evident that, if the blood be uniformly diffused and under the same pressure, it will remain motionless and in equilibrium. When the pressure is changed at any point, as occurs when the left ventricle contracts and throws blood into the arterial system, the blood will move from the part where the pressure is higher to where it is lower; in other words, there will be circulation as a consequence of the difference of pressure. When the heart stops beating, the blood continues to flow more and more slowly until the difference of pressure is equalized, and then there is no circulation. Each stroke of the heart throws as much blood into the arteries as flows into the heart from the veins; the orifices of the veins at the heart are more distensible than the beginnings of the arteries, and consequently the arterial pressure rises more rapidly than the venous pressure diminishes, and thus the beating of the heart raises the mean pressure throughout the arterial system. The circulation is therefore influenced by two factors,—(1) the heart, as regards number, strength, and volume of beats; and (2) the amount of resistance in the arterioles. Modifications of these influences are the pressure and the velocity of the blood.

As the blood is circulating through the vessels under the influence of the action of the heart, it exerts a certain pressure or tension, the existence of which is shown by the jet of blood which spurts out on the puncture of an artery, and the amount of which is indicated by the height to which the jet is propelled. An instrument for measuring this pressure, termed a kymograph, has been devised by Ludwig. But this apparatus, owing to the inertia of the mass of mercury,—the medium used,—can only register mean bloodpressure, and the more delicate variations escape notice. Fick in 1864 attempted to register these smaller fluctuations by means of a curved spring-kymograph, consisting of a hollow spring, which is made to oscillate by variations of pressure communicated to the interior. Small portions of a tracing taken with the mercurial manometric kymograph of Ludwig are shown in fig. 22. From this it will be observed that there is (1) an increase and diminution of blood-pressure with each cardiac beat, as is shown in the smaller curves, and (2) an increase and diminution produced by respiratory movements, the increase occurring chiefly during inspiration and the decrease chiefly during expiration, as is indicated by the larger waves. It is evident also that all the smaller curves have the same general character, and that they reveal nothing as to variation in pressure during individual beats. To show such variations, Fick’s kymograph must be used, when a tracing will be obtained in which slight oscillations of pressure in the down-stroke of each separate beat may be observed. By employing the different forms of kymograph the following conclusions have been arrived at.

(a ) Arterial Pressure.— (1) The pressure diminishes from the heart to the capillaries. (2) It attains its maximum in the ventricle at the moment of systole, and its minimum in the auricle at the moment of diastole, at which time also the pressure in the auricles and in the great veins may be negative, that is, below atmospheric pressure. (3) The mean blood-pressure in the large arteries of large mammals and of man is equal to that of a mercurial column 5 ∙ 5 to 6 ∙ 3 inches in height. (4) The blood-pressure in various animals has been ascertained to be as follows, the results being expressed in terms of a column of mercury of the indicated number of inches in height. Carotid of horse, 6∙34; carotid of dog, 5∙89 (Poiseuille). Carotid of horse, 4 8 to 8∙42; carotid of dog, 5∙89; carotid of goat, 4∙64 to 5∙31; carotid of rabbit, 3∙54; carotid of fowl, 3∙46 to 673; aorta of frog, ∙86 to 1∙14; gill artery of pike, 1∙38 to 3∙3 (Volkmann). Carotid of dog, 5∙12 to 7∙48 (Ludwig). Carotid of calf, 6∙97; carotid of sheep, 6∙65; carotid of goose, 6∙38; carotid of stork, 6∙34; brachial artery of pigeon, 6 ∙ 57 ; carotid of cat, 5∙9; brachial artery of man during operation, 4∙33 to 472 (Faivre). Anterior tibial artery of boy, 3∙93 to 6∙3 (E. Albert). It no doubt varies even in animals of the same species. (5) The arterial pressure at any given point undergoes periodic variations, increasing at the instant of ventricular systole and diminishing during diastole; they are most marked in the arteries near the heart. (6) These periodic variations may be observed in the intermittent spurting of an artery when it is punctured. (7) It is necessary to distinguish between the mean arterial pressure at any point of an artery and the mean pressure of the blood in the whole arterial system, which can only be obtained by taking the mean of the pressures in many different arteries at various distances from the heart. (8) The mean arterial pressure depends directly on the quantity of blood in the arterial system, and consequently on the total calibre of the system, so that any diminution of calibre, produced mechanically or by nervous influences, will increase the mean arterial pressure. (9) The mean arterial pressure increases with the energy of the beats of the heart. (10) The blood-pressure becomes greater with increased and accelerated action of the heart, sometimes with plethora, and after an increase in the amount of blood, such as occurs after a full meal or after transfusion of blood, whilst it becomes smaller during diminished or enfeebled action of the heart, in anaemia, and after haemorrhage or excretions from the blood by the skin, kidneys, or bowels (Landois). (11) The pressure is affected by the degree of contraction or of dilatation of the blood-vessels, according as they are influenced by the nervous system. (12) The pressure is increased in cases of sclerosis or hardening of the arterial walls, in lead poisoning, after injection of ergotin (which contracts the small arterioles) or of digitalis (which acts on the heart), where there is granular or contracted kidney, and in cardiac hypertrophy with dilatation. And (13) the pressure is diminished in fever, in chlorotic anaemia, in phthisis, and by severe haemorrhage.

(b ) Venous Pressure. —(1) In the veins near the heart the pressure is only one twentieth to one-tenth of that of the corresponding arteries. (2) During auricular diastole the pressure in the veins near the heart may become negative ( = - ∙0039 inch of mercury). (3) There are no periodic variations of pressure in the veins as in the arteries, except in the great venous trunks in the neck and near the heart, where there is a diminution of pressure during auricular diastole and an increase during auricular systole. (4) Great activity of the heart diminishes venous, while it increases arterial pressure. (5) The pressure increases in the veins according to their distance from the heart: thus, in the external facial vein of the sheep it is equal to a column of mercury ∙12 inch in height; in the trachial to a column ∙16 inch high; in branches of the trachial, ∙35 inch; in the crural vein, ∙45 (H. Jacobson). (6) Plethora increases venous pressure, whilst anaemia diminishes it. (7) Inspiration causes in the great veins near the heart an increase in pressure, whilst expiration diminishes it; but the respiratory movements “do not affect the venous stream in peripheral veins” (Stirling). (7) Changes in the position of the limbs affect venous pressure hydrostatically: thus, elevation of the extremities favours the flow of blood towards the heart; but, if the heart hangs downwards, the face becomes turgid, as the outflow by the veins is retarded. (8) Gravity favours the emptying of descending and hinders the emptying of ascending veins, so that the pressure becomes less in the former and greater in the latter. (9) As already stated, muscular movement by compressing the veins, aided by the mechanism of the valves, favours the flow of blood towards the heart, and thus increases the pressure in these vessels.

(c) Capillary Pressure.— For obvious reasons capillary pressure has not been directly measured. Von Kries has measured the amount of pressure necessary to occlude the capillaries in an area abounding in these vessels, such as the skin at the root of the nail on the terminal phalanx or on the ear in man, and on the mucous membrane of the gum in rabbits. He found the pressure in the capillaries of the hand, when the hand is raised, to be equal to ∙95 inch of mercury, when it hangs down, 2∙13, in the ear 79, and in the gum 1∙26. Roy and Graham Brown also measured the pressure necessary to close the capillaries in the web of the frog’s foot, in the tongue and mesentery of the frog, and in the tail of newts and small fishes. It is evident that any condition favouring the afflux of blood to a capillary area will increase the pressure in the capillaries, such as the dilatation of the small arterioles conveying blood to an area of capillaries, contraction of the venules carrying off the blood from it, or any increase of pressure in the arterioles or in the venules. The arrangement and position of the capillary network must affect the pressure: the pressure in the capillaries of the glomeruli of the kidney must, for instance, be greater than in those of the skin, as in the former position there is increased resistance owing to the double set of capillaries (see Nutrition, vol. xvii. p. 684). Finally, any change in the degree of contraction of the wall of the capillary itself will affect the pressure.

The general facts regarding pressure in arteries, capillaries, and veins are illustrated by fig. 23.

Various attempts have been made by Volkmann, Vierordt, Ludwig and Dogiel, Hering, and Chauveau and Lortet to measure the velocity of the circulation, and special instruments have been invented for that purpose. In 1850 Volkmann constructed the haemadromometer; this was followed by the haematachometer of Vierordt in 1858 and by the haemadromograph of Chauveau and Lortet in 1867. These instruments are not now much used, having been superseded by the stromuhr (current-clock) or rheometer of Ludwig and Dogiel, which was invented in 1867. This instrument measures the amount of blood which passes through an artery in a given time. It consists of two glass bulbs of equal capacity communicating by a tube. One of the bulbs is filled with oil, which is expelled by the blood into the second (empty) bulb. The instrument is then reversed on its socket so that the bulb containing the blood is farthest from the heart, and the former process is repeated. From the time occupied in filling and refilling the velocity of the blood in the artery of supply can be calculated.

The following figures give, in inches per second, the velocities of the blood in different vessels. Carotid of dog, 8∙07 to 14∙06; carotid of horse, 12∙05; maxillary of horse, 9∙13 metatarsal of horse, 2∙2 (Volkmann). Mean velocity in carotid of dog, 10∙28; in carotid of dog at end of diastole, 8∙46; at end of systole, 11∙69; in crural artery of dog at end of diastole, 5∙51; at end of systole, 9∙41 (Vierordt). During systole in carotid of horse, 9∙84; at time of dicrotic wave, 8∙66; at end of diastole, 5∙9 (Chauveau, Bertolus, Laroyenne). In carotid of rabbits, from 3∙7 to 8∙9; in carotid of dog, weighing 51∙2 ft, poisoned with morphia, from 13∙74 to 28∙86; in carotid of another dog, weighing 26∙69 ft, from 9∙57 to 20∙47; in carotid of dog, weighing 7∙85 ft, in which the sympathetic nerve had been cut, from 8∙03 to 13∙35; and in carotid of another dog, weighing 6∙97 ft, poisoned with morphia, from 13∙35 to 18 03 (Dogiel). The velocity in the capillaries cannot be directly measured. E. H. Weber gives it at ∙032 inch per second in capillaries of mammals and ∙021 in those of the frog. Vierordt gives the velocity in man as ∙024 to ∙035 inch per second. Volkmann states that the flow of blood in mammalian capillaries is five hundred times slower than in the aorta. Donders asserts that the velocity of the current in the smaller arterioles is ten times faster than in the capillaries. When the current reaches the veins it is accelerated in consequence of diminished resistance, but even in the larger venous trunks it is ∙5 to ∙75 times less than in the corresponding arteries. The following general conclusions may be drawn. (1) The velocity of the blood is in inverse ratio to the total calibre of the vessels: rapid in the aorta, it diminishes as we recede from it. (2) Each systole is followed by an increase in the velocity of the blood in the larger vessels. (3) In the smaller arteries, capillaries, and smaller veins the velocity is uniform and constant. (4) The velocity increases in the venous system as we approach the heart. (5) In the large arteries the movements of inspiration retard the velocity, whilst those of expiration increase it. (6) In the large veins the movement of respiration, and also the suction action of the auricle during diastole, cause a rhythmic increase and diminution of the velocity. The explanation of these variations in velocity is obvious. As the arteries pass outwards they give off branches, the united calibre of which is, with rare exceptions, greater than that of the parent vessel. Thus, as Küss expresses it, the arterial system may be regarded as a cone, the base of which ends in the capillaries, whilst the summit is at the aorta; and the venous system is a second cone, the base being also at the capillaries and the apex at the right auricle. Vierordt states that the sectional area of the capillaries is to that of the aorta as 800 to 1; but, as the sectional area of the venous orifices at the heart is greater than that of the arterial orifices, the ratio of the sectional area of the capillaries to that of the veins at the heart has been stated as 400 to 1. The increased sectional area retards the velocity, and the velocity of the bloodcurrent in sections of the vessels at various points is inversely as their calibre. The velocity of the blood does not depend on the mean blood-pressure, and, as was pointed out by Ludwig and Dogiel, the velocity in any section of a vessel depends on (1) the vis a tergo (i.e., action of the heart) and (2) the amount of resistance at the periphery.

It is important to distinguish between the rapidity of the blood current and the time occupied by a blood corpuscle in making a complete circuit through the heart and vessels, say, from the left ventricle to the left ventricle again. Attempts have been made to measure the time, starting from the jugular vein. Hering injected into that vein a few drops of a 2 per cent. solution of ferro-cyanide of potassium, and then examined the blood of the opposite jugular every five seconds by testing with perchloride of iron,—the formation of Prussian blue indicating the moment when the ferro-cyanide made its appearance in the blood of the jugular after having made a tour of the circulation. Vierordt modified the method by examining the blood received from the jugular each half second. The duration of the circulation as thus determined for various animals is as follows,—horse, 31∙5 seconds; dog, 16∙7; rabbit, 7∙79; hedgehog, 7∙61; cat, 6∙69; goose, 10∙86; duck, 10∙64; buzzard, 673; and common fowl, 5∙17 seconds. Vierordt also made the discovery that in most animals the duration of the circulation is equal to the time in which the heart makes about twenty-seven beats. These facts are illustrated in the following table :— [table]

It may also be shown by another method that a volume of blood equal to that in the whole body passes through the heart in about thirty pulsations. Taking the quantity of blood in the body as one-twelfth of the total weight, a man weighing 140 ft contains 11⅔ ft, or 5292 grammes, of blood, which represent in capacity 5302 cubic centimetres. Each beat of the heart throws 172 cubic centimetres into the aorta; therefore the equivalent of the total quantity of blood in the body passes through the heart in about 30 pulsations. Taking the pulse beat at 72 per minute, it follows that the duration of the circulation is about 26 seconds.

It has been satisfactorily proved by Mosso, Von Basch, Dogiel, and François Franck that there is a slight change in the volume of any distensible organ with each beat of the heart. Mosso devised the plethysmograph, an instrument by which the following results have been obtained. (1) The volume of an organ is not fixed, but varies according to the amount of blood contained in it. (2) Its volume changes with each cardiac pulsation, increasing when blood is forced into it and diminishing by the emptying of the capillaries into the veins. (3) Variations in the volume of one or more organs, say, by compression, or by the application of cold, or by the internal administration of substances which affect the calibre of bloodvessels, such as ergot, cause corresponding variations in the volume of other organs. (4) The pulsatile variations are very similar to the pulse-curve, and there are respiratory undulations corresponding to similar variations in blood-pressure tracings. (5) Movements of the limb cause diminution in volume, as was shown by Glisson in 1677, in consequence of acceleration of the venous current. (6) Mental exercise and sleep cause a diminution in the volume of the limb (Mosso). (7) So delicately attuned is the organism that music has been observed to cause a rise and fall in the tracings (Dogiel).

The blood is distributed throughout the body in varying proportions, according to the requirement of any set of organs at a particular time. When any tissue or organ is active, there is a determination of blood towards it, the amount being increased from 30 to 50 per cent.: thus, during digestion the mucous membrane of the stomach and intestinal organs is richly supplied with blood. Increased muscular velocity is always accompanied by increased vascularity; but, whilst this is the rule, there are organs, such as the heart, the muscles of respiration, and nervous centres like those in the medulla oblongata, in which there is a condition of continuous activity, and in which there is a uniform vascularity. Seeing that the activity of certain organs varies at different times, it follows that, whilst some organs are congested, others are at rest. In the child there appears to be a different distribution of blood from what obtains in the adult. The heart of a child is relatively small up to puberty, while the vessels are relatively large; after puberty the reverse is the case. Arterial pressure is less in the child than in the adult, whilst the pressure in the pulmonary circulation is larger in the child than in the adult (Beneke). Attempts have been made to estimate the distribution of blood after death. Ranke states that one-fourth of the total blood is in the muscles, one-fourth in the liver, one-fourth in the heart and vessels, and the remaining fourth in the rest of the organs.

Special Forms of Circulation.

The cranial circulation has been already described under Physiology, vol. xix. pp. 42-43.

The peculiarity of the portal circulation is that the blood passes through two sets of capillaries. Arterial blood is conveyed to the stomach, spleen, pancreas, and intestines by branches of the abdominal aorta. These branches divide and subdivide, terminating in a capillary plexus in the various organs above enumerated. From this plexus the radicles of the various veins spring, and they unite with each other into larger and larger trunks, until by the confluence of the mesenteric veins with the splenic vein the portal vein is formed. The portal vein conveys the blood to the liver, where it divides into smaller and smaller branches constituting a plexus in the lobules of the liver. From this plexus spring the roots of the hepatic vein, which conveys the blood from the liver to the inferior vena cava (see Nutrition, vol. xvii. p. 678). There are thus in the portal circulation two sets of capillaries,—one in the abdominal viscera and the other in the liver. Ligature of the portal vein causes distension of all the abdominal vessels and a highly congested state of the abdominal viscera, whilst the bloodpressure quickly falls, and the animal dies. So distensible are the abdominal vessels that they can contain nearly all the blood in the body. Blood from such congested vessels has toxic properties (Schiff and Lautenbach). The ventricular systole may send a pulse down the valveless inferior vena cava and cause a pulse in the liver. The liver swells with each systole and relaxes with each diastole of the heart.

The pulmonary artery, carrying venous blood, divides and subdivides, and the smallest branches end in a plexus of capillaries on the walls of the air-cells of the lung. From this plexus the radicles of the pulmonary veins originate; and finally the four portal veins, two from each lung, carry the arterialized blood to the left auricle. Considering the apparently small extent of the pulmonary as compared with the systemic circulation, and the fact that the two ventricles, of about equal capacity, empty themselves simultaneously, it is clear that the pulmonary circulation presents many points of interest. In the first place, the pressure in the pulmonary artery is considerably less than that of the aorta. In 1850 it was determined by Ludwig and Beutner to be in the dog equal to a mercurial column of 1∙17 inches, in the cat to one of ∙69 inch, and in the rabbit ∙47 inch, or about three times less in the dog, four times less in the rabbit, and five times less in the cat than the pressure in the aorta. Hering passed simultaneously a tube through the muscular walls of each ventricle of a calf, and the blood rose in the tube in the right ventricle 21 inches and in the left 33∙4 inches (quoted by Landois and Stirling). Fick and Badoud found a pressure of 3∙54 in the pulmonary artery of the dog, whilst the carotid pressure at the same time was 4∙17 inches. The ratio of pulmonary to aortic pressure has been stated as 1 to 3 (Beutner and Marey) and as 2 to 5 (Goltz and Gaule).

Next, it is important to note the peculiar physical conditions in the chest during respiration. As already shown (p. 102), the lungs are distended in consequence of the positive pressure on their inner surfaces being greater than the negative pressure on their outer pleural surfaces. But when the lungs are distended by a full inspiration they exert an elastic force (termed elastic recoil or “elastic traction ”) amounting to about 1∙18 inches of mercury. Outside the lungs, in the cavity of the chest, the surface of the heart and vessels is subjected to a pressure which is the difference between atmospheric pressure (29∙92 inches) and the “elastic traction” (1∙18 inches) or 28∙74 inches. It is clear that the more the lungs are distended the greater is the elastic traction, and consequently the less the pressure on the outer surface of the vessels. The thinwalled pulmonary veins yield more during a deep inspiration, thus diminishing pressure, than the thicker-walled pulmonary artery, whereby the flow of blood from the capillaries of the lung by the pulmonary veins to the left auricle is favoured. On the other hand, expiration by increasing the pressure tends to retard the flow of blood. Further, the velocity of the stream of blood is accelerated in the pulmonary vessels by inspiration and retarded by expiration. As regards the influence of the movements of the lung on the calibre of the pulmonary capillaries and smaller vessels, experiment has shown that the blood-vessels of the lungs containing air and distended are wider than those of collapsed lungs. Suppose an elastic bag having minute tubes in its walls to be dilated in a free space, the lumen of these tubes will be diminished; but, if it be placed in a closed space, as in a wide glass bottle, and if the pressure on its outer surface be diminished by removing air from the space between the bag and the side of the bottle, the bag will distend and the lumen of the tubes will be increased. Thus it is evident that inspiration, by increasing the calibre of the pulmonary vessels, draws blood towards the lungs, and the movements of the lungs become an effective force in carrying on the pulmonary circulation. The velocity of the blood is greater in the pulmonary than in the systemic capillaries, and greater in the pulmonary veins than in the pulmonary arteries. The great degree of distensibility of the pulmonary vessels allows of frequent adjustments being made, so that, within limits, as much blood in a given time will pass through the pulmonary as through the systemic circulation. This adjustment, however, may be readily disturbed. For example, violent muscular exertion hurries the blood along the veins to the right side of the heart, and by the right ventricle the blood is discharged into the pulmonary circulation. If more arrives than can be transmitted to the left auricle by the pulmonary veins in a given time, the pulmonary capillaries become engorged, breathing becomes quick and possibly irregular, the right side of the heart becomes engorged, signs of venous congestion appear in the flushed face and turgid veins, and perhaps the pulmonary capillaries may rupture, causing haemorrhage from the lung. The weaker the muscular structure of the heart the more likely is this to occur. Hence the breathlessness in many cardiac affections, aggravated by muscular exertion, more especially in ascending a stair or hill.

In the mature foetus the fluid brought from the placenta by the umbilical vein is partly conveyed at once to the vena cava ascendens by means of the ductus venosus and partly flows through two trunks that unite with the portal vein, returning the blood from the intestines into the substance of the liver, thence to be carried back to the vena cava by the hepatic vein. Having thus been transmitted through the placenta and the liver, the blood that enters the vena cava is purely arterial in character; but, being mixed in the vessels with the venous blood returned from the trunk and lower extremities, it loses this character in some degree by the time that it reaches the heart. In the right auricle, which it then enters, it would also be mixed with the venous blood brought down from the head and upper extremities by the descending vena cava were it not that a provision exists to impede (if it does not entirely prevent) any further admixture. This consists in the arrangement of the Eustachian valve, which directs the arterial current (that flows upwards through the ascending vena cava) into the left side of the heart, through the foramen ovale,—an opening in the septum between the auricles,—whilst it directs the venous current (that is being returned by the superior vena cava) into the right ventricle. When the ventricles contract, the arterial blood contained in the left is propelled into the ascending aorta, and supplies the branches that proceed to the head and upper extremities before it undergoes any further admixture, whilst the venous blood contained in the right ventricle is forced into the pulmonary artery, and thence through the ductus arteriosus— branching off from the pulmonary artery before it passes to the two lungs—into the descending aorta, mingling with the arterial currents which that vessel previously conveyed, and thus supplying the trank and lower extremities with a mixed fluid. A portion of this is conveyed by the umbilical arteries to the placenta, in which it undergoes the renovating influence of the maternal blood, and from which it is returned in a state of purity. In consequence of this arrangement the head and upper extremities are supplied with pure blood returning from the placenta, whilst the rest of the body receives blood which is partly venous. This is probably the explanation of the fact that the head and upper extremities are most developed, and from their weight occupy the inferior position in the uterus. At birth the course of the circulation undergoes changes. As soon as the lungs are distended by the first inspiration, a portion of the blood of the pulmonary artery is diverted into them and undergoes aeration; and, as this portion increases with the full activity of the lungs, the ductus arteriosus gradually shrinks, and its cavity finally becomes obliterated. At the same time the foramen ovale is closed by a valvular fold, and thus the direct communication between the two auricles is cut off. When these changes have been accomplished, the circulation, which was before carried on upon the plan of that of the higher reptiles, becomes that of the complete warm-blooded animal, all the blood which has been returned in a venous state to the right side of the heart being transmitted through the lungs before it can reach the left side or be propelled from its arterial tranks (Allen Thomson). After birth the umbilical arteries shrink and close up and become the lateral ligaments of the bladder, while their upper parts remain as the superior vesical arteries. The umbilical vein becomes the ligamentum teres. The ductus venosus also shrinks and finally is closed. The foramen ovale is also closed, and the ductus arteriosus shrivels and becomes the ligamentum arteriosum.

The Innervation of BloodVessels.

This has already been described under Physiology (vol. xix. p. 30); but there are several points of interest that can only be thoroughly understood after studying the general conditions affecting, and the mode of measuring, the pressure of the blood. Stimulation of the pneumogastric nerve in the neck slows the rate of the heart-beat, and, if the stimulation be strong, arrests the heart in a state of diastole. Suppose a kymograph to be connected with the carotid in the neck of a rabbit deeply under the influence of chloral so as to be quite unconscious of pain; if then one of the vagi in the neck be stimulated, the blood-pressure curve at once falls; and on removing the stimulation it rises to its former height by a few leaps and bounds. Whilst this occurs in the arteries, the venous pressure rises in consequence of the flow of blood into them from the arteries. But the pressure may be influenced by another method. As was pointed out by Ludwig and Owsjannikow, a centre exists in the medulla oblongata (vaso-motor centre) whence influences emanate that tend to keep the vessels in a more or less contracted condition. If this centre be injured, the smaller bloodvessels throughout the body dilate,—in short, they are paralysed,— and receive more blood, and consequently the pressure in the larger vessels at once falls. This vaso-motor centre in turn can be influenced by impressions reaching it from the periphery. This was clearly proved by Cyon in 1866, when he discovered the function of the depressor nerve, a small nerve (the superior cardiac) originating in the rabbit from the superior laryngeal and from the pneumogastric nerve, but in many animals blended with the pneumogastric nerve. Stimulation of the distal end of this nerve produces no effect; but stimulation of the cephalic end causes a great fall of blood pressure and a diminution in the frequency of the pulse (see Physiology, vol. xix. p. 29 and fig. 11). Similar depressor filaments exist in the trank of the vagus below the origin of the superior cardiac nerve (depressor of Cyon), in the nerves coming from the lungs, in the great auricular nerve, in the tibial, and in all probability in all sensory nerves. Further, it may be influenced by nerve fibres the stimulation of which excites the centre, causing a rise in pressure (pressor nerves). Such filaments have been experimentally demonstrated to exist in the superior and inferior laryngeal nerves, in the trigeminus, and in the cervical sympathetic. The vasomotor centre is therefore under the influence of two antagonistic sets of impulses,—one stimulating it, causing constriction of the smaller vessels and a rise of arterial pressure, the other inhibiting it, causing dilatation of the smaller vessels together with a fall of pressure.

But this is not all. On examining a blood-pressure tracing it is seen that the arterial pressure is influenced by the movements of respiration, the larger waves corresponding to these movements. To ascertain precisely how much of the wave corresponds to inspiration and how much to expiration, suppose a blood pressure taken from the carotid artery, whilst at the same time arrangements are made for recording simultaneously the variations of intra-thoracic pressure. It is then easily seen that, when expiration begins and the expiratory pressure rises the blood pressure rises, while when inspiration begins both fall. Inspiration removes pressure from the outer surface of the vessels and thus allows the walls both of the great veins and of the aorta to distend; but the thin-walled veins yield to a greater extent than the thick-walled aorta. Consequently during inspiration the blood tends to accumulate in the great veins and in the right side of the heart and less escapes by the aorta, and the blood pressure in the aorta falls. On the other hand, during expiration the blood pressure rises, owing to the opposite set of conditions. Roughly speaking therefore, during inspiration blood pressure falls, whilst during expiration it rises. But a careful examination of the curves shows that they do not exactly coincide as to their maxima and minima. Thus the blood pressure rises before the rise of expiratory pressure; or, in other words, during the first part of inspiration there is a fall of pressure and during the second part a rise. This cannot be explained by the mechanical movements of the chest wall, but is caused, partially at all events, by the action of the vaso-motor centre. During the latter portion of the inspiratory period impulses pass from this centre, causing constriction of the smaller vessels, and consequently the rise of arterial pressure observed during this time. Again, an examination of a blood-pressure tracing shows that during the fall of the respiratory curve the smaller curves are larger and fewer in number than during the rise of the curve. After section of the vagi this difference disappears, and it can only therefore be explained by stating that during the first portion of the time of inspiration, and during the fall of arterial pressure, the cardio-inhibitory centre also acts, slowing the beat of the heart. Another important fact showing that the respiratory undulations cannot be accounted for by the mechanical movements of the chest wall is that they appear in a blood-pressure tracing taken during artificial respiration. When a canula is inserted into the trachea and air is forced into the chest by a bellows, it is evident that the mechanical conditions are not those of ordinary respiration. When air is forced in, inflating the lungs to correspond to inspiration, the intra-thoracic pressure is increased instead of diminished as in ordinary respiration, and when the air is sucked out to correspond to expiration the intra-thoracic pressure is diminished instead of being increased as in ordinary expiration; and still the respiratory curves remain. If artificial respiration be suddenly stopped, the blood pressure quickly rises; but this does not occur to nearly the same extent if the spinal Cord be divided. In other words, the rise of blood pressure when artificial respiration is arrested is due to stimulation of the vaso-motor centre in the medulla by the circulation through it of blood too highly venous owing to stoppage of the circulation, as is proved by the fact that, if the influence of the vaso-motor centre be removed, the rise of blood pressure does not take place. Finally, if during artificial respiration both vagi be cut so as to remove the influence of the cardio-inhibitory centre, and respiration be stopped, the pressure will rise as already described, and in a short time a series of undulations will appear in the blood-pressure tracing known as the Traube-Hering curves,— a rising and falling of blood pressure not due to the action of the heart, as they continue even when a pump is substituted for that organ, nor to the movements of respiration, but to a “waxing and waning” of the activity of the vaso-motor centre itself, contracting and dilating the bloodvessels and thus influencing the peripheral resistance. To sum up, the circulation is affected by the nervous system—(1) by the inhibitory action of the vagi in restraining the activity of the heart; (2) by the accelerating action of fibres in the sympathetic, stimulating the activity of the heart; (3) by the action of the intrinsic cardiac ganglia affecting the heart directly; (4) by the action of the vasomotor centre (vaso-constrictor nerves) in the medulla, tending to keep up a greater or less degree of constriction of the vessels; (5) by the action of vaso-dilator nerves inhibiting the vessels, allowing them to dilate in a manner similar to the cardio-inhibitory action of fibres in the vagi; (6) by the influence on the vaso-motor centre of impulses coming from the periphery,—pressor fibres stimulating it, depressor fibres inhibiting it; (7) by the diffusion of impulses in the medulla from the respiratory centres; (8) by the interaction of the vaso-motor, respiratory, and cardio-inhibitory centres in the medulla; and (9) by rhythmic changes in the vaso-motor centre itself. See Physiology, vol. xix. p. 28 sq. Bibliography.— A copious list of works relating to the anatomy of the organs of the circulation will be found in Quain’s Anatomy, edited by Allen Thomson, E. A. Schäfer, and George Dr Thane, 9th ed., vol. ii. p. 916; and on the physiology of the circulation in Beaunis’s Physiologie Humaine, 2d ed., 1885, and in Landois and Stirling’s Text-Book of Human Physiology, 2d ed., vol. i. p. 557. To this last able work, to A. Rollett’s elaborate essay, “Physiologie der Blutbewegung,” in Hermann’s Handbuch der Physiologie, and to Prof. Michael Foster’s Text-Book of Physiology, 4th ed., the author is specially indebted in the preparation of this article. As to the action of drags and poisons on the circulation, reference is made to Lauder Brunton’s Text-Book of Pharmacology, &c., 2d ed., 1886. For a brief account of the historical development of our knowledge of the circulation, see abstracts of lectures by the present writer, delivered before the Royal Institution, in British Medical Journal for 1883. (J. G. Μ.)