Blood-pressure

Front matter

Class.

Book.

Copyright N°_

Preface To The Second Edition

The exhaustion of the first edition of this work in considerably less than two years after publication is a source of gratification and pleasure to the author. In the process of revision for the second edition an increase in size has been necessary in order to include a survey of the constantly growing literature on blood-pressure.

The author has continued his endeavor to present the subject of blood-pressure in a condensed and practical form as definitely as the present state of our knowledge permits. Wherever possible, a summary of the experimental as well as the clinical data available for the consideration of a given topic has been included, together with references to articles upon which statements are based.

As in the earlier edition the chapters upon Physiology and upon Venous Blood-pressure were written by Dr. J. Harold Austin, to whom the author is also indebted for assistance in the preparation of the chapter dealing with the Functional Efficiency of the Circulation. The author's thanks are also due to Miss Eleanor A. Cantner for valuable assistance in the preparation of the charts and drawings, as well as in proof reading.

G. W. N. 1530 Locust St., Philadelphia, 191(5.

Chapter I. The Physiology Of Blood-pressure

By J. HAROLD AUSTIN, M.D.

Definitions. — Blood-pressure is the term used to indicate the pressure exerted by the blood at a given point in the circulatory system at a given moment. Thus we may speak of intra-auricular, intraventricular, arterial, capillary, or venous blood-pressure. When not qualified, the term is used to refer to the arterial blood-pressure, and in man usually to the pressure in the' brachial artery. The arterial blood-pressure is constantly undergoing rhythmic fluctuations due to the cardiac systoles. The highest pressure attained during one cardiac cycle is called the systolic pressure and is attained at the moment of the arrival of the crest of the pulse wave. The lowest pressure attained during a cardiac cycle is called the diastolic pressure. The difference between these two pressures is called the pulse pressure. Thus, if the systolic pressure be 120 and the diastolic 90, then the pulse pressure would be 30. By mean pressure is understood the average pressure at a given point. The mean pressure is not, however, the arithmetical mean between the systolic and diastolic pressures, because the pressure may remain for only a moment at the systolic level, falling very quickly to near the diastolic level and remaining near it throughout the greater part of the average cycle. This is illustrated in the accompanying diagram in which obviously the average pressure lies much nearer to the diastolic than to the systolic.

In addition to the pressure oscillations, dependent upon the cardiac cycle and called oscillations of the first order, there are slower oscillations in the arterial pressure dependent upon the respiratory movements. These are called blood-pressure oscillations of the second order. Finally, still slower oscillations, usually over ten to 2 twenty cardiac cycles, occur. These are due to various factors, among which rhythmic variations in the activity of the vasoconstrictor centre or in the cardiac activity are the most important. These constitute the oscillations of the third order. All three types of oscillations are shown in the tracing (see Fig. 6).

-S = systolic pressure ; D = diastolic pressure ; average pressure.

M

The pressure which is exerted by the blood against the vessel wall while the current flows unobstructed through the vessel is known as the lateral pressure. The pressure exerted by the blood against an obstruction in the lumen of the vessel is known as the end pressure. The end pressure exceeds the lateral pressure at any given point, and the difference is the pressure that is effective in producing the blood-flow at that point. The accompanying diagram

Fig. 2. — Illustrating lateral pressure: 1, 2, 3, 4, 5, lateral pressure at points along outflow tube; h, the difference between lateral pressure and end pressure at any point. (From Howell.)

(Fig. 2) illustrates the relation between lateral and end pressures. End pressure in a branch artery is shown to be approximately equal to the lateral pressure in the mam trunk at the point at which the branch takes origin. The method used commonly for the measurement of blood-pressure in man shows the end systolic

METHODS OF MEASUREMENT pressure in the brachial artery and the lateral diastolic pressure. 1 Blood-pressure is usually expressed in millimeters (sometimes centimeters) of mercury above or below the atmospheric pressure at the same point. Thus blood-pressure of 120 is a pressure that will sustain in addition to the atmospheric pressure at the point, the pressure of a vertical column of mercury 120 mm. high.

Fig. 3. — M, mercury manometer; F, float; G, perforated cap; P, recording pen; C, cannula for insertion into vessel; w, washout tube, shown in detail at B; R and E, for introduction and outflow of magnesium sulphate solution; both are clamped off while recording pressures. (From Howell.)

Methods of Measurement. — The first exact measurements of blood-pressure were published by the Rev. Dr. Stephen Hales, an Englishman, in a little book entitled Statical Essays, in 1733. He meas-

'A. K. Cushny, Zentralbl. f. Physiol., Leipsic u. Wien, 1907-8, xxi, 77; N. D. Straschesto, Archiv f. d. ges. Physiol., Bonn, 1909, cxxviii, 1.

ured the pressure in the femoral artery of a horse by connecting it with a glass tube and noting the height to which the blood rose in this tube held vertically. In 1828 Poiseuille applied the mercury manometer to the study of blood-pressure and in 1847 Ludwig invented the recording manometer with moving drum. Ludwig's method is essentially the one used today in physiological experiments. A manometer is connected by tubing filled with some fluid which will inhibit coagulation, such as saturated magnesium sulphate solution, with a cannula introduced into the artery. A manometer so connected gives a record of the end pressure in the artery.

In physiological work the mean pressure is obtained by constricting the communication between the manometer and the vessel

Fig. 4. — Diagram of Hiirthle manometer. Tubing from heart or vessel to small tambour T, both filled with fluid. Movements of tambour magnified by compound lever S, and transmitted to writing pen. (From Howell.)

to a small opening. This prevents the transmission of the faster blood-pressure oscillation to the manometer, and leads to the production of a straight line representing the average or mean pressure. In studies upon man the mean pressure cannot thus be directly recorded and is, in fact, difficult to determine. All pressures determined upon human beings are therefore, as a rule, either systolic or diastolic pressures. It is the custom of some authors to speak of that pressure which is half-way between the systolic and diastolic pressures in man as the mean pressure. This seems to us misleading, inasmuch as it may in certain cases be considerably above the true mean pressure. Dawson 1 has shown that the mean pressure in man is usually obtained by adding approximately one-third of the

METHODS OF MEASUREMENT pulse pressure to the diastolic pressure. For the measurement of the systolic and diastolic pressures in physiological work, Hurthle devised the membrane manometer which is shown in Fig. 4, since the inertia of the column of mercury in the mercury manometer is too great to give an accurate record of the rapid fluctuations.

To the artery

Fig. 5. — Maximum-minimum manometer. When cock a is open and b closed, the highest pressure attained during the period of record is transmitted to the manometer and retained by the maximum valve. When a is closed and b opened, the mercury falls to the lowest pressure occurring in the period of record and is retained there by the minimum valve.

Another method in use in physiological work for the control of the membrane manometer is the so-called valve manometer, or maximal-minimal manometer. This is illustrated in Fig. 5. By using one valve or the other, either the highest or the lowest pressure occurring within a given interval of time is recorded. The maximal pressure recorded by such a manometer is not, however, identical with the systolic pressure, nor the minimal with the diastolic pressure. This may be seen by referring to Fig. 6. The maximal-minimal manometer will record the highest or lowest pressure attained over a certain period of time, and this is usually long enough to admit the occurrence of all three orders of pressure oscillations. It would i n mmin 1 1 1 1 1 1 1 1 1 i i n 1 1 i i i 1 u nin \ i it i 1 1 1 n 1 1 1 mm i n n n i rWtAA/v/W^ v ^ATMAr vv ,/^/'A

<vVv

Base Line

20 mm

Babbit

Fig. 6. — Diagram illustrating at Bp a typical blood-pressure curve dampened by constricting the communication between the artery and the manometer so as to reduce the amplitude of the shortest waves. Shortest waves, cardiac; longer waves, respiratory; longest waves (three in the tracing), waves of third order. T, time record in seconds. (From Howell.)

seem desirable, therefore, to use the terms maximal and minimal pressures in this sense. Certain authors, however, have used these terms as synonymous with systolic and diastolic pressures respectively.

Measurements of the blood-pressure in the smaller arterioles and capillaries either in man or in animals must be made by other methods, and are described in a later chapter.

Venous pressure is measured, in physiological work, in the same way as the arterial, but usually with a water manometer rather than with a mercury manometer. A pressure of 34 cm. II 2 is equal to a pressure of 25 mm. Hg. Blood-pressure within the heart is measured by introducing an oiled cannula, either through one of the vessels or through a puncture wound, into the chamber within which the pressure is desired.

BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE.

The blood-pressure in an individual varies with the point of the cardiovascular system under consideration, its elevation with respect to the heart, and with the phase of the heart, whether systole or diastole. These variations are indicated in Table I, which gives approximate systolic and diastolic pressures in different parts of the cardiovascular system at the level of the heart in man. That the blood-pressure varies greatly in different parts of the vascular system has long been known, the marked difference in the force of the stream flowing from a cut artery and from a cut vein being a striking illustration.

Table I. — Approximate Pressure in Cardiovascular Tree op a Normal Man, Aged Twenty Years, at Level op Heart.

In mm. Hg.

Systolic. Diastolic.

Left ventricle 150 to 200

Brachial artery 105 to 140 80 to 110

Radial artery 95 to 125

Arterioles 80 to 95

Medium capillaries 50 to 60 50 to 60

Smallest capillaries 20 to 35 20 to 35

Smallest veins 20 to 30 20 to 30

Large vein of arm 1 to 15 1 to 15

Right ventricle 25 to 60

Pulmonary artery 25 to 60 15 to 25

This table is extremely diagrammatic and is intended merely to emphasize certain facts. It will be noted that the chief fall in pressure occurs between the smaller arteries and the capillaries, that is, in the arterioles; furthermore, that this affects the systolic pressure more than the diastolic, so that under normal conditions the pressure in the capillaries shows no pulse wave. When the arterioles are widely dilated this fall of pressure, especially of systolic pressure, in them is diminished and an appreciable pulse may penetrate into the capillaries. Under these conditions the systolic pressure in the capillaries approaches that in the smaller arteries, and the diastolic pressure in the arteries approaches that of the capillaries. It will further be noted that any increase in venous pressure must promptly elevate the capillary pressure. Indeed, the capillary pressure is more readily raised by venous stasis than by increased arterial pressure.

In the recumbent position the lateral pressure throughout the entire length of the aorta is very nearly constant. In the upright position, however, the pressure at the lower end of the aorta is higher than the pressure at the arch, by the weight of the column of blood separating the two points; approximately 2 mm. Hg. per inch.

In the veins the pressure is largely dependent upon posture, i. e., upon the height of the point measured above or below the right auricle. At the right auricle the pressure is probably about to 10 mm. Hg., varying with the phase of respiration, and that in the trunk is about 2 mm. higher for every inch below the heart; in the lower extremities, however, the venous pressure, while high, is not so high as this calculation would indicate (see p. 135). This relation leads to some distention of the veins in the lower and dependent portions of the body, while the veins of the upper portion of the body are but partially filled.

The Factors that Maintain and Regulate Blood-pressure. — The cardiovascular system may be considered from this point of view as consisting of six elements. (1) The heart, the source of energy. (2) The arteries acting as elastic vessels, dilating to receive each new ventricular delivery of blood, and contracting to maintain during the filling and resting periods of the heart an even flow through the capillaries. (3) The capillaries, the site of active functionation of the blood and with the smaller arterioles the chief source of the resistance in the circulation. (4) The veins which with the capillaries serve as a reservoir, maintaining a pressure just sufficient to fill promptly the relaxing heart for its next systolic contraction. (5) The blood itself, the incompressible, inelastic medium which fills the cardiovascular system. (6) The lymphatic system with its tissue spaces, serous cavities and lymphatic channels filled with lymph, acting as an additional but less promptly available reservoir for body fluids.

The Heart. — The heart is the chief source of the energy that maintains the blood-pressure. The factors that affect the heart's efficiency to this end are the factors that influence the output of blood per minute from the heart. They are as follows: (1) The diastolic filling of the ventricles; this is dependent upon (a) the venous pressure, (b) the length of diastole, and (c) the cardiac tone. (2) The completeness of systolic emptying. (3) The number of beats per minute, or cardiac rate. (4) The efficiency of the valves of the heart. The cardiac cycle may be divided into two parts: (1) systole, or the period of cardiac contraction, (2) diastole, or the period of cardiac relaxation and rest. The ventricular systole and diastole are each further subdivided. The first one-third or onefourth of the ventricular systole is occupied in raising the pressure within the ventricle, from the pressure produced by the auricular systole to the diastolic pressure of the pulmonary artery or of the aorta. This is the so-called presphygmic period or " anspannungszeit." When this pressure is attained the semilunar valves open and, with the propulsion of the blood onward into the aorta, the pressure rises in both ventricle and aorta to the systolic pressure. This pressure is then maintained in the ventricle almost to the end of systole, driving the blood at an even rate out into the aorta and into the smaller vessels. With the relaxation at the close of systole the pressure in the ventricles falls to zero as the semilunar valves close. Diastole now commences. The venous pressure causes the tricuspid and mitral valves to open and the blood fills the ventricles at a rate dependent upon the venous pressure. The amount of distention produced in the ventricle by a given venous pressure is determined by the cardiac tone — the greater the tone, the less the distention. When this inflow is completed the diastole proper ends and the remainder of the cycle is occupied by a period of rest or diastasis.

With changes in cardiac rate, the duration of both systole and diastole are altered, but the former much less than the latter. The length of the systole in man, with a pulse rate of about 75 to 95, is from 0.3 to 0.38 second. With slow rates that permit time for adequate filling of the ventricles Henderson, 1 Bohr 2 and Putter 3 have found that providing an adequate venous pressure is maintained, the systolic discharge is under normal conditions practically a constant quantity for any given individual, and the changes in the rate influence only the duration of diastasis. Hence the cardiac output per minute under such conditions will be proportional to the cardiac rate. With a more accelerated pulse rate, however,

2 Skand. Arch. f. Physiol., 1909, xxii, 221. 3 Ztschr. f. klin. Med., 1911, lxxiii, 342.

Henderson has shown that the ventricle has not sufficient time to receive its full quota of blood and the diastole is shortened. In consequence, the systolic discharge is diminished, and although the volume output per minute still increases as the pulse becomes more rapid, it falls farther and farther behind proportionally. Henderson holds to the view that the systolic output of the heart is determined entirely by two factors — the cardiac rate, altering the duration of the diastole, and the venous pressure. On the other hand, Zuntz 1 and Plesch 2 find evidence to support the view that, in addition, the heart is capable of varying its output per minute independently of the rate and of the venous pressure, as the result of direct changes in the cardiac tonus and in the amplitude of the cardiac stroke.

Henderson and Barringer have found that with normal cardiac tonus the venous pressure necessary to distend the right ventricle as rapidly as it relaxes is not more than 5 mm. of water in excess of the intrathoracic pressure. This he calls the critical venous pressure. Studies upon the dog and man have led him to the view that while normally the pressure in the intrathoracic veins may during a very deep inspiration become less than atmospheric, it never normally becomes less than 45 mm. of water above the intrathoracic pressure and therefore falls scarcely, if at all, below the critical pressure. In normal inspiration, the descent of the diaphragm, by compressing the abdominal capillaries and veins, somewhat increases the venous flow into the thorax.

In an athlete, panting after a contest, not only the inspiratory descent of the diaphragm, but also the powerful expiratory contraction of the abdominal muscles must hasten the venous flow from the splanchnic area to the right auricle, and aid in maintaining the critical venous pressure in spite of the accelerated cardiac rate and hence increased cardiac output. It is probable that in extreme tachycardia, the shortening of diastole and consequent imperfect filling of the ventricle may actually lead to a diminished cardiac output per minute.

Henderson and Prince 3 from a study of the oxygen pulse (the oxygen consumption by the body per minute divided by the pulse rate) with varying amounts of work, have concluded that the systolic discharge of a well-developed man, working hard and with a pulse rate of 140 per minute, is not less than 100 c.c. of blood.

i Ztschr. f. klin. Med., 1912, lxxiv. 347. 2 Ztschr. f. Physiol., 1912, xxvi, 90.

s The Oxygen Pulse and the Systolic Discharge, Am. Jour. Physiol., 1914, xxxv, 106.

Venous Pressure. — So long as an adequate venous pressure is maintained, the cardiac output per beat is probably dependent upon the duration of diastole. x\t slow and normal cardiac rates, the diastolic filling is complete, but at accelerated rates the filling becomes progressively diminished. Inadequate venous pressure reduces the cardiac output. On the other hand, in the presence of a dilated heart an abnormally high venous pressure probably tends to keep the ventricles overdistended, thus establishing a vicious cycle.

Cardiac Rate. — At slow and moderate rates the cardiac output per minute is probably proportional to the cardiac rate. At more rapid rates the minute output increases with the pulse rate, but not proportionally. At extremely rapid rates imperfect ventricular filling may probably actually diminish the minute output.

We may sum up the effects of these factors as follows:

Cardiac Tone. — Either unduly diminished cardiac tone, by permitting dilatation of the ventricles, or unduly increased cardiac tone, by interfering with the diastolic filling, impairs the cardiac output.

Stenotic or incompetent valves tend to diminish the cardiac output, although this defect is at first compensated by increased amplitude of contraction and frequently by increased rate.

Of these various factors, changes in one may to some extent be compensated by changes in another. Elevation of venous pressure may be counteracted by increase of cardiac tone. On the other hand, no changes in cardiac activity can compensate a deficient venous return resulting from hemorrhage, from stagnation of the blood in the widely dilated peripheral vessels (vasomotor shock), or from some mechanical obstruction to the venous flow. The reflex acceleration of the cardiac rate that results is usually ineffective.

Marey noted that increased blood-pressure is followed by slowing of the pulse, and later Eyster and Hooker 1 showed that this is due to vagus stimulation occurring reflexly when the blood-pressure in the carotids or the aorta is increased, even though changes in the cerebral circulation be excluded. The action of the vagus upon the heart is to diminish the cardiac rate by reducing the activity of the "pace-maker," and therefore to decrease the output per minute, and when extreme, to reduce the conductivity of the auriculoventricular bundle, producing partial or complete block.

1 Zentralbl. f. Physiol., Leipsic u. Wien, 1907, xxi, 615.

Roy and Adami 1 have shown by cardiometer studies that with increased aortic pressure, even though the output per minute may be increased, the residual blood (that remaining in the ventricles at the end of systole) is increased and the ventricles become more widely dilated during diastole. Excessive aortic pressure therefore leads to loss of ventricular tone, with dilatation and impairment of cardiac efficiency.

Arteries. — The elasticity of the arteries, by virtue of which they dilate during each systole to accommodate the ventricular output with only a moderate rise of the pressure within them, and then during diastole contract again, forcing a continuous stream through the capillaries and maintaining under normal conditions a fair pressure throughout diastole, is a property of the utmost importance. Without this elasticity the strain upon the cardiac muscle would be enormously increased, as would be the strain during systole upon the vessel walls. Were the heart pumping into an absolutely rigid system, the cardiac systole would be prolonged, the systolic pressure enormously increased and the diastolic pressure would fall to zero, with a cessation of flow during diastole. The pulse pressure would equal the systolic pressure. Such an extreme condition never actually exists, but some approach toward it may be seen in individuals with sclerotic arteries in whom often a systolic pressure of 200 may be associated with a diastolic pressure of 130; a pulse pressure, therefore, of 70, as contrasted with the normal pulse pressure of about 30. Obviously this exaggeration of the pulse pressure by rigid vessels will be less marked if the cardiac rate be increased and the output per beat correspondingly diminished. The pulse pressure is not infrequently looked upon as a rough measure of the cardiac activity. This to some extent it is; yet we have just seen it is influenced also to a marked degree by the condition of the arteries. It has been commonly accepted that this elasticity of the arteries, while it results from the tonus of their muscular coats, is to be looked upon as a passive elasticity not unlike that of a rubber tube. Hasebroek 2 has, however, recently advanced the hypothesis that while the dilatation of the arteries is a passive result of the injected volume of blood, their contraction is an active muscular act and, indeed, an important adjunct to the heart in the maintenance of blood-pressure and blood-flow. He believes this active arterial contraction to be the chief cause of the dicrotic wave of the sphygmogram.

1 British Med. Jour., 1SSS, ii, 321.

2 Deutsch. Archiv f. klin. Med.. 1911, eii, 567.

Arterioles, Capillaries, and Veins. — The smaller arterioles together with the capillaries constitute the main resistance in the circulation, and are chiefly responsible for the proper distribution of the blood-flow to various organs and tissues, as the relative demands of these for blood changes with altering activity. The blood which reaches the smaller arterioles at a mean pressure, but little below that in the aorta, leaves them at a very low pressure, varying with the portion of the body under consideration. Whether this fall of pressure occurs chiefly in the small arterioles or in the capillaries is a matter of dispute. The capillaries together with the veins of the body serve as a reservoir for the blood. Complete loss of tone in these vessels leads to the accumulation in them, particularly in the splanchnic region, of practically all the blood in the body. The capillary and venous tone is therefore responsible for maintaining the supply of blood to the right auricle and this, as we have already seen in considering the heart, is of the utmost importance for the maintenance of cardiac output and of blood-pressure.

The Vasomotor System. — In this relation it is the capillaries and veins of the splanchnic area that are of greatest significance. This was shown experimentally by Ludwig and Thiry 1 in 1864. These vessels alone are capable of containing all the blood of the body and were they to lose their tone the individual would promptly " bleed to death in his own vessels," as in vasomotor shock. In certain of the lower animals the tone of these vessels is relatively low. The hutch rabbit can be killed by simply holding it by the ears in the vertical position, the splanchnic vessels not having sufficient tone to overcome the force of gravity. In the dog manual pressure over the abdomen will cause a prompt rise of carotid blood-pressure of 20 or 30 mm. of mercury due to the forcing of the blood from the vessels onward to the right auricle. The regulation of the tone of the arterioles, capillaries, and perhaps veins, is the most important factor toward this end. This is brought about by the vasomotor nervous system. The vasomotor system consists of two main parts, the vasoconstrictor system and the vasodilator system.

The Vasoconstrictor System. — The first important experimental studies upon this subject were those of Claude Bernard. 2 In 1851 he noted the dilatation of the vessels in the ear of the rabbit after cutting its cervical sympathetic nerve on the same side. Later he

1 Quoted by Howell, Text-book of Physiology, Philadelphia, 1912; Sitz. d. kais. Akad. d. Wiss. math, naturw. CI., 1864, xlix, 2, p. 442.

2 Legons sur les liquides de l'Organisme, Paris, 1859.

observed that electrical stimulation of the upper end of the cut nerve caused constriction of these dilated vessels. Thus was demonstrated the existence of vasoconstrictor nerves.

The vasoconstrictor system consists of a centre in the medulla which is connected with the vessels of the body by nerve paths, each consisting of three neurons. In the medulla beneath the middle of the fourth ventricle exists the bilateral nerve centre which is chiefly responsible for the maintenance of vasomotor tone. This centre is continuously in a state of tonic activity which at times undergoes rhythmic fluctuations, giving rise to the Traube waves, to be described. Porter has recently found evidence against the view that both the arterial tonus and the vasomotor reflexes following stimulation of afferent nerves are controlled by the same master cells, the so-called vasomotor centre. He has been able by the use of curare in cats to more than double the sciatic and the depressor reflex change in blood-pressure, while the arterial tonus is left substantially unchanged. Possibly, therefore, we may be compelled to recognize two centres, a vasotonic and a vasoreflex centre, related but separable. 1 The axons leading from these medullary cells pass down the cord to end around cells of the anterior horn, from the upper thoracic level to the upper lumbar, and constitute, with the medullary cell, the first neuron. The axons of the anterior horn cells are medullated and constitute the second neuron in the chain, the so-called preganglionic fibers. They pass from the cord in the white rami communicantes from the first thoracic to the second or fourth lumbar segments, and entering the sympathetic chain, have one of three destinations. Those destined for the extremities end around cells in the sympathetic chain. The non-medullated fibers of these sympathetic cells constitute the third neuron, the postganglionic fibers. They pass by the gray rami communicantes back to the spinal cord and thence accompany the appropriate spinal nerves to their destination. The preganglionic fibers destined for the deeper vessels of the head pass through the white rami of the first to sixth thoracic segments and up the sympathetic to the superior cervical ganglion. From this point the associated postganglionic fibers are distributed through the carotid and other vascular plexuses. The preganglionic fibers destined for the vessels of the abdominal and pelvic viscera, the most important of all in the regulation of blood-pressure, pass directly through the sympathetic

1 Am. Jour. Physiol., 1914-15, xxxvi, 418.

chain and by way of the splanchnic nerves to the celiac, inferior mesenteric, or other large prevertebral ganglia. From these ganglia the postganglionic fibers are distributed to the plexuses around the abdominal vessels. Section of the first neuron in this chain, as by section of the cervical cord, leads to extreme loss of vascular tone with fall in blood-pressure, failure of the circulation, and death. If the circulation be, however, artificially maintained after section of the cervical cord, the spinal cells, the second neurons, gradually assume a moderate tonic activity and restore a very imperfect vascular tone. This may in turn be destroyed by destruction of the spinal cord. Finally, Goltz 1 has shown that even after destruction of the cord, some vascular tone may be recovered which must be attributed to tonic activity either of the third postganglionic neuron or of the musculature of the vessel wall. Excitation of the vasoconstrictor centre with contraction of the peripheral vessels is called forth by the stimulation of pressor fibers, which may be demonstrated in almost any large nerve containing afferent fibers, but especially in the cutaneous nerves. These pressor fibers may be stimulated by electricity, by cold applied to the skin, and in other ways. Depression of the centre with diminished contraction of the vessels is called forth by stimulation of other afferent fibers, called depressor fibers. These likewise may be demonstrated in many of the large afferent nerves. Thus, application of warmth to the skin leads to local vascular dilatation, the result of stimulation of depressor fibers. Sensory stimuli from certain regions, notably the middle ear and the testis, give rise, as a rule, to depressor effects. Electric stimulation of the central end of the cut sciatic or of the splanchnic nerve may lead to either pressor or depressor effects.