Reprinted from the American Journal of Physiology. 
Vol. I. March i, 1898. No. 11. 
THE INFLUENCE OF THE HEART-BEAT ON 
THE FLOW OF BLOOD THROUGH THE 
WALLS OF THE HEART. 
W. T. PORTER. 
[From the Laboratory of Physiology in the Harvard Medical 
School.] THE 
American Journal of Physiology 
VOL. I. 
MARCH i, 1898. 
NO. 11. 
THE INFLUENCE OF THE HEART-BEAT ON THE 
FLOW OF BLOOD THROUGH THE WALLS 
OF THE HEART.1 
W. T. PORTER. 
[From the Laboratory of Physiology in the IJarvard Medical School.] 
IN 1689 J. Baptista Scaramucci2 published two hypotheses which 
have played a great part in the history of the physiology of the 
heart: the first, that the deeper coronary vessels are squeezed empty 
by the contraction of the muscle fibres which surround them; and 
the second, that the coronary vessels are refilled from the aorta dur- 
ing the diastole of the heart. In 1707, Stroem3 added to these the 
hypothesis that the coronary vessels are filled in diastole because 
their mouths are closed in systole by the semilunar valves. Thus, 
almost at the outset, the penetrating conception of Scaramucci was 
linked with an obstinate and overshadowing error, destined to be a 
source of controversy for nearly two hundred years.4 Thebesius, 
1 The first account of my observations on the compression of the intramural 
vessels by the systole of the heart was published in the Journal of the Boston 
Society of Medical Sciences, No. 10, March 30, 1897. Most of the facts have 
been presented also to the American Physiological Society, in Washington, May 5, 
1897, and to the British Association for the Advancement of Science, Toronto, 1897. 
2 Scaramucci : Diario Parmense, 1689. Quoted by Haller : Element, physi- 
ology 1778, lib. iv, s. v, p. 459. 
3 Stroem : Nova theoria machinae animalis. Quoted by Haller : loc. cit. 
4 A sufficient account of the literature of this subject has already been given by 
Ceradini, G. : II meccanismo delle valvole semilunari del cuore. Milan, 1871 ; 
Der Mechanismus der halbmondformigen Herzklappen. Leipzig, 1872. See also 
Rebatel, F. : Recherches experimentales sur la circulation dans les arteres 
coronaires. Paris, 1872. IV. T. Porter. 
146 
Vieussens, Morgagni, Boerhaave, and other famous eighteenth cen- 
tury men took sides for and against the theory of Stroem, and not 
until the century had passed, and many observers of the first 
rank had shown that the mouths of the coronary arteries are often 
beyond the reach of the semilunar valves, and that the pulse in these 
vessels is synchronous with the pulse in the aorta, did opinion come 
to rest on the filling of the coronary arteries in both systole and dias- 
tole. The calm that followed was brief indeed. About 1840, Mar- 
shall Hall attempted to revive the old belief, but was answered by the 
experiments of Kleefeld. Five years after Kleefeld, the controversy 
broke out afresh. Briicke on the one side and Hyrtl on the other, 
neither knowing that he was repeating arguments and observations 
that already filled many pages of cardiac literature, fought over the 
old ground, drew many with them into an extended and often un- 
profitable discussion, and reached the old conclusion. Once more 
physiological opinion settled to the belief that the coronary arteries 
are filled during systole as well as diastole, a position since ren- 
dered impregnable by the observations of Ceradini and the experi- 
ments of Rebatel and of Martin and Sedgwick. 
Throughout this long discussion, the primary hypothesis of Scara- 
mucci, namely, that the deeper coronary vessels are emptied by the 
squeeze of the fibres contracting around them, received but scant 
attention. Thebesius,1 in the celebrated inaugural dissertation in 
which he gave the first accurate description of the cardiac veins 
that bear his name, had said that in “no way could the arterial 
blood be forced into the vessels of the heart, unless during diastole; 
because in systole, the contraction of the fibres is so intense that all 
blood would be forced out, from the arteries no less than from the 
veins, a condition that actually can be observed in the hearts of 
amphibia—frogs and others which appear all white and bloodless 
when contracted, but are red and swollen with blood when relaxed in 
diastole; ” and such reasoning was accepted by many who forgot that 
the heart of the frog is almost wholly wanting in bloodvessels, and 
that the red color of the full ventricle is due to the blood which 
fills the ventricle, seen through its translucent walls. 
After the middle of the present century, experiment grew bolder 
and speculation began to yield place to direct observation. Hyrtl,2 
in 1855, trying to prove that the coronary arteries were filled in both 
1 Thebesius ; De circulo sanguinis in corde. Leiden, 1708, p. 14. 
2 Hyrtl : Ueber die Selbststeuerung des Herzens. Vienna, 1855, p. 9. Influence of Heart-beat on Flow through Heart-Walls. 
147 
systole and diastole, severed a coronary artery in the living rabbit, cat, 
and dog, and declared positively that only the upper segment spurted 
in systole, —a statement confirmed by Peris.1 In 1876, King 2 drew 
a ligature about the rabbit’s heart at the auriculo-ventricular junction 
while the heart was in full systole, and again while in diastole. He 
then coagulated the blood in the cardiac vessels by holding the organ 
some time in dilute sulphuric acid, and compared thin sections of the 
ventricle with regard to the amount of blood in their walls. The 
vessels of the heart ligated during diastole were filled with blood, 
while those of the heart ligated during systole contained little blood. 
But neither of these experiments can be said to be of value in our 
present inquiry: for the observation of Hyrtl, though accurate for 
his purpose, which was to determine which limb of the severed artery 
“ spurted,” is otherwise incorrect; and the method of Klug is open 
to objections based upon facts discovered since his time. 
With regard to Hyrtl’s work, it is true that the distal segment of a 
severed coronary artery does not “ spurt,” but it is also true, as will 
be shown in detail in the description of the writer’s experiments, that 
blood is forced out of the distal segment with each contraction of the 
ventricle. The quantity which thus escapes is extremely small, but 
this is because the amount of blood contained in the distal segment 
of a severed “ terminal ” artery is always necessarily small. The 
anastomosis with neighboring vessels is too slight to permit of col- 
lateral circulation, and only a free collateral circulation can cause the 
distal end of a severed artery to bleed profusely. 
Turning to Klug’s experiment, let us consider first the heart ligated 
in systole. Klug slowed the heart in order to be sure of the moment 
of ligation. The reader will not need to be reminded that when the 
beat of the mammalian heart is considerably slowed by exhaustion, or 
by artificial means, as in Klug’s method, the cavity of the ventricle is 
seldom, if ever, fully emptied. The observations of Pratt3 have 
shown the ease with which the veins in the heart wall are filled from 
the cavity of the ventricle through the vessels of Thebesius. It is 
clear that even if a ligature could be drawn tight around the auriculo- 
ventricular junction in the precise fraction of a second during which 
the mammalian heart remains fully contracted, the relaxation of the 
1 Perls, M. : Archiv fur pathologische Anatomic, 1867, xxxix, p. 189. 
2 Klug, F. : Centralblatt fur die medicinische Wissenschaften, 1876, p. 134. 
3 Pratt, F. H.: The nutrition of the heart through the vessels of Thebesius 
and the coronary veins. American journal of physiology, 1898, i, p. 86. W. T. Porter. 
148 
ventricle after the tying of the ligature would fill its capillaries from 
the ventricular cavity, so that the amount of blood in the ventricular 
walls when the heart came to be examined would in no wise corre- 
spond to the amount present in the walls at the height of their con- 
traction. If the heart is permitted to beat at its usual rapid rate, the 
ventricular cavities may be fully emptied at each stroke; but the time 
for the tying of the ligature is then so short that it is obviously impos- 
sible to be sure whether the ligation is made in full systole or a little 
before or after systole. If it were possible to be sure of the moment 
of ligation, and to make certain that the ventricular cavities were 
empty at that moment, and that the ligature shut off the auricles 
entirely, the mural capillaries could still be filled when the heart 
relaxes from the blood in the large superficial coronary vessels, which 
are not within the grasp of the contracting fibres and cannot be com- 
pressed by them. In the heart ligated in diastole, it cannot be deter- 
mined whether the blood found in the intramural vessels was present 
there at the moment of ligation, or entered the walls afterward through 
the veins of Thebesius or the superficial coronary vessels. Finally, the 
plunging of the fresh heart, warm from the body, into a coagulating 
bath of sulphuric acid, may so change the tonus of the ventricle as to 
alter materially the amount of blood in its capillaries. These sources 
of error render the observations of Klug unavailable. 
It is Rebatel1 whom we must thank for the first fruitful experi- 
ment in this field. Chauveau had given him the circulation in the 
coronary arteries as the subject of his inaugural dissertation, and had 
suggested that a T-tube should be placed in the right coronary artery 
of the horse and connected with an haemodromograph, which should 
write a curve of the quickness of flow in the coronary artery, while at 
the same time a curve of the tension in the aorta should be recorded 
for purposes of comparison. Rebatel secured these curves, and saw 
at a glance that the beginnings of the upstrokes in the aortic and the 
coronary curves coincided exactly, showing that the blood-wave is 
synchronous in the two arteries, and that the coronary arteries are 
filled during systole. He saw also that the primary increase in the 
rapidity of current in the coronary artery was followed by a second 
augmentation “ corresponding exactly to the moment when the aortic 
tension is least, i. e., to the diastole of the heart. The first augmen- 
1 Rebatel, F. : Recherches experimentales sur la circulation dans les arteres 
coronaires. Paris, 1872. Influence of Heart-beat on Flow through Heart-Walls. 
149 
tation,” Rebatel asserts, “ is evidently due to the propulsion imparted 
to the column of liquid by the contraction of the ventricle; the sec- 
ond current may be due to the entrance of a new wave from the aorta 
Fig. 1. Curves of the tension in the aorta (upper tracing) and the quickness of flow in the 
right coronary artery of the horse, simultaneously recorded (Rebatel’s Fig. 3, page 25). 
into the coronary artery, or to a sudden diminution of the peripheral 
resistance in the intramural vessels (p. 27).” To determine the origin 
of the second current, the tension and the quickness of flow in the 
coronary artery were recorded simultaneously. It was then seen that 
the tension curve was like that of every other artery, and presented no 
secondary rise or other feature that could account for the secondary 
augmentation in the quickness of flow. Thus led to a variation in the 
peripheral resistance, Rebatel concluded that the primary blood-wave 
Fig. 2. Curves of the tension and quickness of flow in the right coronary artery of the 
horse, simultaneously recorded (Rebatel’s Fig. 8, page 29). 
penetrates with difficulty into the intramural branches during systole, 
because of their compression by the contracting cardiac muscle, but 
when the relaxation of the ventricle opens the peripheral vessels, the 
pent stream rushes suddenly forwards, and thus produces the second, 
or diastolic, rise in the curve of the haemodromograph. 150 
IV. T. Porter. 
Rebatel himself does not accept this hypothesis unreservedly. His 
attitude is that of M. Marey,1 who, on being shown the curves, admitted 
that the first proposition, namely, the filling of the coronary arteries 
in systole, is incontestable, while the second, namely, that the increase 
in quickness of flow is due to the opening of the intramural vessels by 
the relaxation of the ventricle is only “ very probable and legitimately 
deduced.” An analysis of Rebatel’s tracings (Fig. 2) suggests that 
even this qualified approval was incautious. The extraordinary arti- 
ficial irregularities in these curves at once attract attention. The 
curves are defaced by huge after-vibrations and inertia errors. The 
shock of the primary wave drives the writing levers far beyond 
the real maximum of the upstrokes; there is then a sharp rebound, 
which, in several instances, carries the writing points far below the 
correct level of the curve. Evidently the lever of the haemodromo- 
graph, once set in motion by the sudden and violent changes in pres- 
sure and velocity consequent on the beat of the heart, has continued 
to swing. Serious as these faults are, they are by no means the chief 
reason for doubting the correctness of Rebatel’s reasoning. Accord- 
ing to him, the second augmentation is caused by the relaxation of 
the ventricle opening the compressed intramural vessels. But this 
relaxation occurs in the first half of the cardiac cycle, as shown by 
the position of the dicrotic notch in those of his tension curves that 
are written clearly enough to make the dicrotic notch visible. Hence, 
the maximum of the second augmentation, according to the hypothe- 
sis, should occur at the moment when the compressed vessels are 
opened by the swiftly relaxing ventricle, and not shortly before the 
ventricle contracts again, as in the curves before us. The delay can- 
not be explained by the sluggishness of the recording apparatus, for 
Rebatel assures us that the primary waves of tension and quickness 
are synchronous. 
The form of the wave supposed to indicate a second augmentation 
of the rate of flow is still less reconcilable with Rebatel’s hypothesis. 
The alleged increase in velocity quickly reaches its maximum, and is 
always succeeded by a rapid fall, greater in many of the tracings than 
the rise which precedes it. In the absence of any change in the blood- 
pressure either in the aorta or in the coronary arteries, it is impos- 
sible to understand how this slowing in the blood stream can take 
1 M. Marey, que nous remercions d’avoir bien voulu examiner nos traces, 
admet, ainsi que nous, la premiere proposition comme incontestable, et la seconde 
comme tres-probable et legitimement deduite (p. 31). Influence of Heart-beat on Flow through Heart- Walls. 
151 
place. If a reservoir containing water kept at a constant level and 
provided with an elastic outflow tube is raised 130 cm. above the 
mouth of the tube, thus giving a constant pressure like that of the 
blood in the coronary arteries, shown to be constant by Rebatel’s 
tension curves, and the mouth of the tube compressed, as the tubes 
of the coronary system are said by Rebatel to be compressed, and 
then released, while the water flowing out during two brief successive 
periods is measured, it will be found that the outflow per unit of 
time, or in other words the velocity, is even a little greater in the 
second period than in the first. His second augmentation should, 
therefore, not have been followed by a marked slowing in the rate 
of flow. 
Thus, seeing that Rebatel’s second augmentation of velocity is not 
synchronous in his own curves with the relaxation said to be its cause, 
and perceiving that the form of the curve offered by him in evidence 
is physically improbable under the conditions premised by him, we 
may conclude that his results do not prove his assumption that the 
intramural vessels of the heart .are compressed in systole. 
I have spoken thus fully of Rebatel’s work both because of its 
intrinsic interest and because his are the only recorded experiments 
that bear directly upon the problem in hand. It is true that Martin 
and Sedgwick,1 ten years after Rebatel, recorded simultaneously curves 
of the blood-pressure in the carotid artery and in a branch of the left 
coronary artery ; but their tracings were taken with a mercury manom- 
eter, and show nothing more than the synchronism in the primary 
pulse-wave, finer details being obscured by the inertia of the mercury. 
My own observations upon the characters of the coronary pulse 
began Sept. 16, 1895, with the record of the pressure-curve in the 
carotid and left coronary arteries in the dog. It seemed a priori 
probable that variations in the peripheral resistance in the coronary 
arteries would be visible in the pressure-curve, provided it were 
written with a sensitive manometer. 
The heart of a dog anaesthetized with ether was exposed, the 
ramus descendens of the left coronary artery ligated about two centi- 
metres from its origin, and a cannula tied into the central end. The 
1 Martin, H. N., and W. T, Sedgwick: Journal of physiology, 1882, iii. 
p. 165. W. T. Porter. 
cannula was then connected by thick-walled but flexible rubber tubing 
to a glass tube, which led to a sensitive Hurthle membrane manom- 
eter, placed on the level of the artery. Evidently a manometer thus 
situated must receive the pressure-changes in the ramus circumflexus 
of the left coronary artery and in the branches given off by the ramus 
descendens in the first part of its course, i. e., between its origin and 
the cannula. A second manometer recorded simultaneously the 
changes of pressure in the carotid artery. But the hope of securing 
a curve from the coronary arteries differing from the pressure-curve 
Fig. 3. Sept. 16, 1895. Curves of the blood-pressure in the left coronary artery (upper 
tracing) and the carotid artery (lower tracing) of the dog, recorded simultaneously. 
One half the original size. The horizontal line below each curve is the line of 
atmospheric pressure. In the case of the carotid artery, the atmospheric pressure 
line served also for the record of the time, in fifths of a second. The intervals of the 
graduation-scales correspond to a pressure of 20 mm. Hg. On raising the pressure in 
the Hiirthle manometers to 100 mm. Hg, as here recorded, and then opening the 
chamber of the manometer to the pressure of the atmosphere, the writing points re- 
turned accurately to the line of atmospheric pressure, this line in the pressure-scale 
being thus twice drawn. The vertical lines are synchronous ordinates. During the 
latter part of the curves, the heart was slowed by vagus excitation. 
of other arteries was not realized. The most careful scrutiny of the 
two curves taken during the ordinary contractions and during the 
slowing of the heart by vagus excitation (see Fig. 3) failed to reveal 
any noteworthy difference, except that the pulse-wave reaches the 
coronary artery sooner than the carotid, depending of course on the 
nearness of the former vessel to the heart. 
The first fully satisfactory evidence of the effect of the contraction 
of the ventricle on the flow of blood through the walls of the heart 
was secured during the writer’s experiments on extirpated portions 
of the ventricle of the dog and cat. When a piece of the mammalian 
ventricle is kept beating by supplying it with defibrinated blood Influence of Heart-beat on Flow through Heart- Walls. 
153 
through its nutrient artery at a constant pressure, each beat can be 
seen to force the blood out of the severed vessels in the margins of 
the fragment. The details of several of these experiments are as 
follows: 
Experiment March 2Q, iBgy. A dog weighing 11 kilos, anaesthetized 
with morphia and ether, was bled from the left carotid artery, and the blood 
whipped, filtered through glass wool, and diluted with an equal volume of 
0.8 per cent normal saline solution. Normal saline of the same strength was 
meanwhile allowed to flow into the right jugular vein. After a short interval, 
the dog was again bled from the carotid artery. A second injection of saline 
solution was followed by a third bleeding. The product of these bleedings 
was mixed, and placed in a reservoir at the temperature of the body. The 
heart was now extirpated, and a cannula tied into the ramus descendens of 
the left coronary artery not far from the apex of the left ventricle. That 
part of the apex which could be fed through the cannula was then excised. 
Both apex and basal portion fibrillated. The septum was removed. The 
piece of ventricle secured was 28 mm. in length (/. e. the direction from the 
base to the apex), 23 mm. broad opposite the end of the cannula, and 27 
mm. broad at the somewhat flattened tip of the apex. The ventricle meas- 
ured from base to apex 70 ram. The cannula was now connected with the 
blood reservoir and the apex perfused with blood. In a few moments regu- 
lar and strong contractions set in. Curves were recorded with an ordinary 
muscle lever. The flow of blood from the veins was increased during each 
systole. The experiment was stopped after the apex had contracted one 
hour and forty minutes. During a part of this time the preparation was in a 
bath of blood at the temperature of the body. 
March 30, iBgy. On the morning of this day, a cannula was placed in 
the ramus descendens of a dog prepared as in the foregoing experiment, and 
most of the left ventricle and all of the right ventricle and septum except a 
fringe near the arteria descendens cut away. The portion remaining was fed 
through the cannula with defibrinated dog’s blood, and beat strongly and at 
first quite regularly. It was observed that the outflow from the veins was 
increased at each systole. Distinct pulsations synchronous with the con- 
tractions of the heart-fragment were observed in the vena descendens at the 
point where it crosses the auriculo-ventricular groove. A cannula was tied 
into this vein, and a pulsation of the liquid in the cannula noted. 
Api'il 5, iBgy. A pulse synchronous with systole was observed in the 
liquid in a cannula placed in the coronary artery of a piece of dog’s ventricle 
fed with defibrinated blood from a reservoir at a constant pressure. 
April g, ißgy. The circumflex area of the left ventricle of a cat’s heart 
was fed with defibrinated cat’s blood at a constant pressure through a cannula 154 
IV. T. Porter. 
placed in the ramus circumflexus. A vein on the surface of the ventricle was 
incised, and a little stream of normal saline solution allowed to flow over the 
opening, so as to prevent the blood collecting there. By this means a clear 
view of the wound in the vein and the escaping blood was secured. The 
discharge from the vein was then seen to be distinctly greater with each con- 
traction of the ventricle. The superficial veins in a fragment of the auricle 
left attached to the preparation were observed to be nearly obliterated by 
each systole of the auricle. The pulse in these auricular veins could not 
have been caused by the rhythmic contractions of the coronary sinus, for the 
pulse in the veins continued after their separation from the sinus. More- 
over, a similar pulse, noted in the superficial ventricular veins, ceased when 
the ventricle stopped beating, although the coronary sinus continued to 
contract. 
The effect of the contraction of the heart on the contents of the 
intramural vessels can also be demonstrated in the living animal, as 
the next experiment will show. 
Api'il 12, iBgy. A dog weighing 24 kilos was anaesthetized with mor- 
phia and ether, and the heart exposed by the resection of a part of the first 
five ribs on the left side. A branch of the vena descendens was incised 
about midway between the base and the apex of the ventricle, and a small 
stream of warm 0.8 per cent normal saline solution allowed to flow over the 
spot in order that the wound and the quantity of blood escaping from it 
might be readily seen. The vagus was now divided in the neck, and the 
peripheral end stimulated with induction shocks of such a strength that the 
ventricle was not continuously inhibited, but still gave occasional beats. 
Each time the ventricle contracted, the blood gushed from the vein. The 
increased outflow appeared absolutely synchronous with the contraction. 
An eye-witness of this experiment could hardly have been per- 
suaded that the gush of blood from the vein in systole was due to 
the transmission of the arterial pulse wave through the capillaries 
into the veins, yet it seemed advisable to answer this possible objec- 
tion by direct experiment. 
July 22, ißgy. The experiment of April 12 was this day repeated, and 
again each contraction of the ventricle caused a greatly increased outflow 
from the vein. The vagus inhibition being prolonged, the heart swelled 
greatly, and the occasional contractions which broke through the inhibition 
were very strong. Each of these powerful contractions caused the blood to 
spurt from the vein. The heart was now excised, and the aorta connected 
with a reservoir of defibrinated dog’s blood much diluted with 0.8 per cent Influence of Heart-beat on Flow through Heart- Walls. 
155 
NaCl solution. The pressure in the reservoir was about xoo mm. Hg, so 
that, as soon as the connection with the aorta was made, the blood from the 
reservoir filled the artery, closed the semilunar valves, and passed through 
the coronary vessels. The perfused heart beat for a few minutes with con- 
siderable strength. With each beat the wound in the vein spurted, as an 
artery spurts when severed in the living animal. 
The following experiments show that the squeezing of the vessels 
by the contracting muscle fibres makes itself evident in the arteries as 
well as in the veins. In this connection, it should be remarked once 
more, that the coronary arteries are “ terminal arteries.” In the 
absence of a collateral circulation, any pulsation observed in the 
distal segment of a coronary artery after its ligation is probably due 
to the compression of the intramural vessels by the contraction of 
the heart, and not to the transmission of an arterial pulse through 
collateral branches from other arteries. 
Novernber 18, 1897. A dog was anaesthetized with morphia and ether, 
and the heart exposed by the resection of the first five ribs on the left side. 
The ramus descendens was then ligated about 20 mm. from its origin. The 
artery was now incised 10-12 mm. distal to the ligature. A little blood 
escaped from the wound. On stimulating the vagus so that the ventricle 
contracted only occasionally, and allowing a small stream of warm normal 
saline solution to flow over the opening, it was possible to see plainly that 
each beat forced blood out of the artery. There was no visible delay between 
the beat and the outflow. The artery was now tied a few millimetres distal 
to the wound. The slight flow from the artery then ceased altogether, but 
during each systole a little blood appeared at the mouth of the wound in 
the artery. 
The next day, a very high constant pressure was suddenly made 
in the aorta of a living dog, so that the semilunar valves were kept 
closed for a time, the pressure on their aortic side being greater than 
the maximum pressure in the left ventricle. The coronary circula- 
tion was fed during this time not by the beat of the ventricle but by 
the blood in the pressure-reservoir. Nevertheless, each beat of the 
ventricle forced blood out of the incision made in a coronary vein on 
the surface of the ventricle and out of a wound made in the arteria 
descendens distal to a ligature which had been placed around it. 
The details are as follows: 
November ig, ißgy. The great vessels and heart of a dog anaesthetized 
with morphia and ether were exposed by resecting five ribs on the left and 156 
W. T. Porter. 
three ribs on the right side and removing the upper part of the sternum. 
Cannulas were placed in the right and left carotid arteries. The right sub- 
clavian artery was ligated at its origin, and the left subclavian artery and the 
aorta prepared so that they could be clamped at the proper moment. The 
cannula in the left carotid artery was connected with a reservoir containing 
0.8 per cent NaCl solution at a pressure of 140 mm. Hg. The cannula in 
the right carotid was connected to a mercury manometer, which showed a 
maximum pressure of 51 mm. Hg (the heart being rather feeble from long 
exposure). A vein on the surface of the left ventricle was now incised. 
The venous blood escaped from the wound in weak jets synchronous with the 
contractions of the ventricle, which were infrequent enough to permit the 
outflow to be seen distinctly. The stopcock between the carotid artery and 
the reservoir of saline solution under pressure was now opened and the left 
subclavian artery and the aorta clamped. The pressure in the manometer 
connected with the right carotid artery then rose to more than double its 
former maximum height. The semilunar valves were kept shut by this very 
high pressure in the aorta. The left ventricle, unable to open the semilunar 
valves, became greatly distended. An observation on the outflow from the 
incised artery and vein was made the moment the high pressure in the aorta 
closed the semilunar valves, before there could possibly have been time for 
the heart-beat to change sufficiently to overcome a pressure nearly three times 
as great as the former maximum arterial pressure, if indeed it could ever have 
done so. The blood still emerged from the vein in gentle systolic jets. The 
wound in the artery merely oozed, but the quantity escaping was distinctly 
greater in systole. 
The emptying of the intramural vessels by the systolic squeeze 
of the fibres around them has been repeatedly observed in this 
Laboratory in the course of experiments on the extirpated heart of 
the cat, and has recently been admirably demonstrated by my friend, 
Mr. F. H. Pratt, by suspending a strip of the cat’s heart, fed through 
one of the coronary arteries, in a large vessel of normal saline solu- 
tion. The experiment is so instructive that it seems worth while 
to describe in this place a simple method by the aid of which the 
phenomena may be very easily shown. 
A cat is anaesthetized with ether and cannulas placed in the left 
carotid artery and the right jugular vein. The animal is now bled 
from the artery. When the blood no longer flows except in drops, 
the artery is clamped, and 0.8 per cent NaCl solution at a tempera- 
ture of 370 C. allowed to flow slowly into the jugular vein. When 
the blood vessels are well filled with saline solution, the cat is bled Influence of Heart-beat on Flow through Heart-Walls. 
157 
again. The blood drawn in the first bleeding is diluted one half with 
the normal saline solution. The defibrinated blood mixture from 
both bleedings is then placed in a Mariotte tube, 30 cm. long and 
3 cm. in diameter, of 190 c.c. capacity. The Mariotte tube opens 
below into a vertical glass tube about 5 mm. in diameter, on the end 
of which is a cannula provided with a stopcock. The cannula is 
inserted in the ramus descendens or the ramus circumflexus of the 
left coronary artery and all the heart cut away except that part of the 
ventricle supplied by the chosen artery. The fragment of the ven- 
tricle is now suspended in a very large beaker, filled with warm nor- 
mal saline solution. When the Mariotte tube, the connecting tube, 
and the cannula are filled with the defibrinated blood, the height of 
the liquid column is about 65 cm., giving a blood-pressure of about 
50 mm. Hg in the coronary artery. On opening the stopcock 
between the cannula and the upright tube, the blood circulates 
through the coronary artery and its branches, and the fragment of 
ventricle presently begins to beat. With each contraction the blood 
shoots from the severed vessels in the margins of the fragment some 
distance into the surrounding liquid, making a funnel-shaped cloud 
in the clear saline solution. 
Having thus demonstrated the pressure which the muscular fibres 
in the heart exercise upon the intramural vessels during systole, it 
remains to consider to what extent this constriction and subsequent 
relaxation assist the flow of blood through the heart walls. That 
they do assist the flow of blood through the heart walls seems a priori 
probable ; it is, indeed, difficult to imagine how the periodical squeez- 
ing of vessels communicating on the one hand with the aorta, a res- 
ervoir in which the pressure is always relatively very high, and on the 
other with outflow channels in which the pressure is always relatively 
very low, could fail to drive the blood towards the point of low 
pressure, i. e. into the veins. But these premises do not justify the 
conclusion that the systolic compression of the intramural vessels 
increases the total volume of the coronary circulation. This is quite 
another problem, and one which cannot be answered from the data 
thus far brought forward. It has just been demonstrated that the 
circulation through the intramural vessels is diminished during the 
contraction of the fibres around them. The emptying of the vessels 158 
W. T. Porter. 
and their subsequent refilling is favored by this same rhythmic con- 
traction. Which of these factors has the upper hand? Does the 
check which the circulation through the walls sustains during systole 
diminish the total volume of blood passing through the wall per 
minute, or is the lessening more than made up by the favorable fac- 
tors the emptying of the intramural vessels and -their easier re- 
filling? The experiments next to be described afford a partial answer 
to this question. 
In February, 1896, while studying with Messrs. Magrath and Ken- 
nedy the relation of the volume of the coronary circulation to the 
frequency and force of the ventricular contraction in the isolated 
heart of the cat, I observed that the heart took more blood through 
the coronary arteries from a reservoir under constant pressure when 
contracting than when at rest. The same observation was made 
again, later in that year, when at work with Miss Hyde on the effect 
of the distention of the ventricle on the flow of blood through the 
walls of the heart. The fact is very well demonstrated by Fig. 4. 
Fig. 4. Showing the increase in the volume of the coronary circulation consequent on 
an increase in the force of ventricular contraction. The uppermost tracing is the 
pressure in the left ventricle of the isolated heart of the cat, recorded by a Hlirthle 
manometer ; the next is the time, in seconds ; and the lowermost is the record of the 
drops of blood flowing through the coronary vessels. The arrow points to the dis- 
tention of the ventricle, which shortly calls forth beats of greater force. From an 
experiment performed with Miss I. H. Hyde. 
In this experiment the extirpated heart of a cat was fed with warm 
defibrinated cat’s blood from a reservoir at constant pressure through 
a cannula in the ascending aorta, all the branches of that vessel ex- 
cept the coronary arteries having previously been tied. The blood Influence of Heart-beat on Flow through Heart-Walls. 
159 
passed from the coronary artery into the right ventricle, and thence 
through a glass tube, drop by drop, onto an aluminium plate fas- 
tened upon the lever of a Marey tambour.1 The variation in the air 
pressure in the tambour occasioned by the falling drops was trans- 
mitted through a connecting tube to a second tambour, provided 
with a small chamber, thin membrane, and very light moving parts, 
and recorded by its writing lever upon the smoked paper of a kymo- 
graph. With this record of the number of drops of blood passing 
through the coronary vessels was written the pressure in the left 
ventricle, the cavity of which was filled with normal saline solution 
and connected with a sensitive Hurthle membrane manometer. A 
side branch led from this cannula to a Mariotte flask placed higher 
than the heart and filled with normal saline solution. When the 
stopcock leading to this flask was opened, the pressure in the left 
ventricle rose, as shown by the rise in the base line of the curve. 
After a few seconds the stimulus of the increased intracardiac pres- 
sure caused the ventricle to beat with greater force and the volume 
of the coronary circulation became greater, and this in spite of a 
diminished frequency of contraction. Later, the pressure in the ven- 
tricle was lowered to that of the atmosphere, the ventricle contracted 
less vigorously, and the volume of the coronary circulation was 
correspondingly reduced. 
A diminution in the volume of the coronary circulation in conse- 
quence of lessening the frequency of contraction is demonstrated by 
Fig. 5. The uppermost curve in this figure records the pressure in 
the left ventricle of the isolated heart of the cat, fed through the aorta 
and coronary vessels with defibrinated cat’s blood at a constant pres- 
sure and temperature. The ventricle was filled with saline solution 
and connected with a Hurthle membrane manometer. The second 
curve was written by the armature of an electro-magnet placed in the 
primary circuit of a du Bois-Reymond inductorium. The heavy 
white line records the stimulation of the peripheral end of the vagus 
nerve with a weak induced current; the individual strokes of the 
armature are blended, owing to the slow speed of the smoked paper. 
The third curve marks the number of drops of blood flowing through 
the coronary vessels, the recording apparatus being that used for 
the experiment illustrated by Fig. 4. The fourth curve marks the 
time in seconds. The weak excitation of the vagus diminished the 
1 For the details of this method and a discussion of its sources of error, see 
Magrath and Kennedy : Journal of experimental medicine, 1897, ii, p. 13. 160 
W. T. Porter. 
frequency of ventricular contraction, but left the force unchanged. 
The volume of the coronary circulation lessened when the frequency 
of contraction lessened, and was restored with the restoration of the 
former frequency. 
Fig. 5. March 26, 1896. Showing the lessening in the volume of the coronary circula- 
tion consequent on a lessening of the frequency of the heart-beat. The uppermost 
tracing is the pressure in the left ventricle of the isolated heart of the cat; the line be- 
low was drawn by the writing point of an electro-magnet placed in the primary cir- 
cuit of the inductorium, the broad, white band indicating the duration of vagus 
stimulation; the next curve records the number of drops of blood passing through 
the coronary vessels; and the lowermost tracing is the time, in seconds. The weak 
excitation of the vagus finally lessens the frequency of contraction, at once the 
volume of the coronary circulation is also lessened. 
It would seem, then, that an increase in either the force or the 
frequency of the contractions of the heart increases the volume of 
blood passing through the coronary circulation by means of the 
periodical emptying of the intramural vessels, yet it would not be 
prudent to accept this conclusion unreservedly. Two possible sources 
of error suggest themselves. The recorded changes in the volume 
of the coronary circulation may depend upon alterations in periph- 
eral resistance in consequence of changes in the tonus of the heart 
muscle, or they may be due to changes in the vascular tonus in 
consequence of the action of vasomotor nerves. ihe first of these 
sources of error may be excluded with considerable certainty. The 
base line of the intraventricular pressure curves in Figs. 4 and 5 
gives no evidence of changes in tonus; Fig. 5 is particularly con- 
vincing. The possible action of vasomotor nerves cannot be wholly 
excluded. Yet the pronounced synchronism between the changes Influence of Heart-beat on Flow through Heart- Watts. 
161 
in frequency and the changes in the volume of the coronary circu- 
lation in Fig. 5 points toward a mechanical explanation, and seems 
to warrant the statement that the increase in the volume of the cor- 
onary circulation which accompanies an increase in the force or 
frequency of the heart-beat is probably to be explained by the peri- 
odical emptying of the intramural vessels by the contraction of the 
heart. 
It is conceivable that the emptying of the intramural vessels by the 
contraction of the heart may favor the flow of blood through the 
heart walls in two ways: first, by the diminished resistance which 
the empty patulous vessels should offer to the inflow of blood from 
the aorta when the heart relaxes; and second, by the suction which 
might accompany the sudden expansion of the compressed vessels, —- 
expanding either by virtue of their intrinsic elasticity, or because of 
the pull of the surrounding tissues upon their walls, as the heart 
quickly regains its diastolic form. It will be best to begin with the 
second problem, namely, the possible suction of the relaxing heart 
muscle. 
The method by which this problem was attacked consists in sud- 
denly connecting the distal portion of a coronary artery of the 
strongly beating heart with a small reservoir of blood at the atmos- 
pheric pressure. If each compression of the deeper branches of the 
artery were followed by an expansion sufficient to cause a note- 
worthy suction, the blood in the reservoir should be drawn into the 
artery; for this blood is the sole source of supply throughout the ex- 
periment, the “ terminal ” nature of the coronary arteries preventing 
any material backflow from collateral branches. It will be seen from 
the experiments about to be cited that no appreciable suction can be 
demonstrated in the larger coronary arteries, even when a very sensi- 
tive minimum valve is interposed between the artery and the reser- 
voir in order to prevent the possible masking of the suction by rising 
pressures accompanying the contraction of the ventricle. 
April 14, 1897- The heart and great vessels of a dog anaesthetized with 
morphia and ether were exposed by the removal of a part of the chest wall. 
A glass cannula, 177 mm. long and 3.5 mm. in diameter, bent near the end 
as illustrated by Fig. 6, and furnished with a stopcock and a side branch 
leading to a minimum manometer, as shown in Fig. 7, was connected with a 162 
IV. T. Porter. 
reservoir containing warm defibrinated dog’s blood, obtained in the manner 
described in the Exp. March 29, page 153. The pressure in the blood reservoir 
was maintained at a constant level of about 80 mm. Hg. 
(The exact reading of the mercury manometer connected 
with the reservoir was inadvertently omitted from the pro- 
tocol.) The minimum valve and its manometer were 
filled with 0.8 per cent NaCl solution, and the cannula 
and the connecting tubes with defibrinated dog’s blood. 
The long cannula was now rapidly passed through the 
innominate artery, aorta, and left coronary artery into 
the ramus circumflexus, which it filled completely, and 
the stopcock leading to the blood reservoir opened. The 
stopcock leading to the minimum manometer had pre- 
viously been closed. The defibrinated blood entered the 
arterY at about the normal temperature and pressure and 
maintained a satisfactory circulation. The heart con- 
tinued to beat strongly and regularly. The blood reser- 
VQ-r was now suddenly shut off, and the stopcock leading 
to t^ie minimum manometer as suddenly opened. Ihe 
contents of the manometer passed slowly into the artery, 
Fig 6 Lower end 
of glass cannula 
fer perfusing the 
ramus circum- 
flexus in the liv- 
ing animal 
but on comparing the level of the liquid in the manometer, with that of the 
heart it was found that the ma- 
nometer was higher than the 
heart. The slow emptying of 
the manometer may therefore 
have been due to gravity. The 
experiment shows at least that 
there is no strong suction, other- 
wise the manometer would have 
been emptied rapidly. 
April is, 1897• The fore- 
going experiment was repeated, 
but no suction could be demon- 
strated. 
April 16, 1897. The experi- 
ment was varied by tying a can- 
nula into the ramus descendens, 
opened for the purpose on the 
surface of the ventricle near the 
origin of the artery, and connect- 
Fig. 7. Minimum valve and cannula, one- 
fourth actual size. 
ing this cannula with a minimum manometer, filled, as before, with normal 
saline solution. But no suction could be found. Influence of Heart-beat on Flow through Heart-Walls. 
163 
April 2j, 1897. A cannula tied into the ramus descendens of a dog’s 
heart was furnished with a T-tube, one limb of which led through a minimum 
manometer to a nearly horizontal glass tube filled with normal saline solution, 
while the other led to a reservoir from which the descendens area was sup- 
plied with warmed, defibrinated dog’s blood at about the normal pressure 
(Fig. 7). While the heart was beating well, the descendens area being fed 
from the pressure flask, the latter was suddenly cut off and the stopcock 
leading to the minimum valve tube opened. There was no suction, although 
the conditions of the experiment were all favorable to its discovery. 
Experiments similar to that of April 16 on the dog have been tried 
on four cat’s hearts (Nov. 11—17), but also without finding any suction. 
It should be remarked that these are all negative results. Against 
a single positive result they would be worthless. Yet lam obliged 
at present to conclude that the relaxation of the heart wall does not 
produce a suction in the larger coronary vessels. 
Having failed to demonstrate any suction in the coronary arteries 
during the diastole of the heart, it is necessary to accept the alterna- 
tive explanation of the favorable influence of the heart-beat on the 
flow of blood through the heart-walls, namely, the diminished resist- 
ance which the empty patulous vessels offer to the inflow of blood 
when the heart relaxes. 
Summary. 
I. Curves of the blood-pressure in the carotid and the coronary 
artery, recorded simultaneously by two sensitive membrane manome- 
ters, reveal no noteworthy difference in the form of the pulse-wave. 
2. The intramural branches of the coronary vessels are compressed 
by the contraction of the muscle fibres around them. 
3. The volume of blood passing through the coronary vessels is in- 
creased by an increase in either the force or the frequency of the heart- 
beat. 
4. It is probable that this increase in the volume of blood passing 
through the coronary vessels is accomplished largely through the 
periodical emptying of the intramural vessels by the systolic squeeze 
of the fibres around them. 
5. The emptying of the intramural vessels by the contraction of 
the heart favors the flow of blood through the heart-walls chiefly by 
the diminished resistance which the empty patulous vessels offer to 
the inflow from the aorta when the heart relaxes. 
6. The relaxation of the heart-walls does not produce a note- 
worthy suction in the larger coronary vessels.