Download Effect of Plethora and Hemorrhage on Left Ventricular Volume and

Effect of Plethora and Hemorrhage on Left
Ventricular Volume and Pressure
By J. P. HOLT, M.D.,
PH.D.
With the collaboration of J. Allensworth, J. Diana, David Collins and Jfelga Kines
By combining conventional methods for recording pressures from the left ventricle and pleural
cavity with a new procedure for estimating end-diastolic volume (EDV) and end-systolic volume
(ESV) of the left ventricle it was found in the closed-chest dog that plethora increased EDV,
ESV and stroke volume while hemorrhage had the opposite effect. There were linear relationships between EDV and ESV, and between EDV and stroke volume. There was little change in
left ventricular "effective" end-diastolic pressure when the EDV changed over a wide range, beginning with the smallest EDV consistent with life; but after a certain large EDV had been reached,
large increases in effective end-diastolic pressure were associated with little or no further increase
in EDV.
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mental conditions.5 It was hoped that the
studies described here would bring evidence to
bear on these points.
W
ITH the development of the electric
conductivity method for estimating enddiastolic volume (EDV), end-systolic volume
(ESV), and stroke volume of the left ventricle,1
it became of interest to determine the relationship between these factors and other circulatory factors in dogs subjected to a wide
variation of EDV, ESV, and stroke volume
such as occurs following plethora and hemorrhage. Since the applicability of Starling's law2
has never been studied in the intact, closedchest animal by measuring the volume of an
individual ventricle, it was desirable that these
studies be carried out. Although it is generally
agreed that Starling's law of the heart is an
important concept describing one of the basic
properties of heart muscle, evidence has been
presented in recent years that under certain
circumstances other factors may at times play
an important role in the regulation of the
heart's contraction.3 Kor instance the tone of
the heart muscle may change,4 and the heart
may operate at one energy level at one time
and at another level under different environ-
METHODS
hi the anesthetized closed-chest dog (morphine,
dial urethane,* phenobarbital), a large radio-opaque
ureteral catheter was passed through the carotid
artery and the ascending aorta into the left ventricle
in such a manner that the tip of the catheter lay
approximately in the middle of the ventricular
chamber. A single lumen electric conductivitycatheter,1 containing the electric conductivity cell at
the end of the catheter, was passed through the
other common carotid artery into the ascending
aorta within a few millimeters of the aortic valve. In
some cases a double lumen electric conductivity
catheter,1 was similarity introduced so that one of
the catheter tips lay in the ventricular cavity and
the other in the ascending aorta near the aortic
valve. Their location was judged by the form of
pressure tracings obtained with a Statham strain
gage, and were verified at autopsy. Use of a fluoroscope was not found necessary. The EDV, ESV,
and stroke volume of the left ventricle were determined as previously described. Approximately 1.5
ml. of 4 per cent NaCI solution were injected "instantaneously" into the left ventricle and the electric
conductivity of the blood in the archof the aorta was
measured. A continuous record of the pressure within
the left ventricle was recorded by means of either a
Brush electromagnetic ink-writing oscillograph or a
Hathaway photographic oscillograph using a Brush
amplifier. While ventricular pressure recording was
discontinued for approximately 1 sec. the 4 per cent
NaCI solution was injected "instantaneously" into
From the Institute for Medical Research, University of Louisville, Louisville, Ky.
This work was supported in part by grants from
the National Heart Institute, USPHS, and the
American, Kentucky and Louisville Heart Associations.
A preliminary report of this work was presented
at the meeting of the American Heart Association in
Cincinnati, Ohio, on October 29, 1956.
Received for publication January 29, 1957.
* Kindly supplied by Ciba Pharmaceutical Products, Inc.
2/3
Circulation ifrsroyrh, I'olutne V. Mar/ /fl.i~
274
PLETHORA AXD HEMORRHAGE ON LEFT VENTRICULAR VOLUME ANO PRESSURE
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the left ventricle. Immediately following this injection the pressure within the ventricle was recorded
for several seconds. In this way a record of intraventricular pressure was obtained at the time of the
measurement of the EDV. Intrapleural pressure was
usually measured by means of a metal cannula inserted between the ribs over the left side of the heart
and connected to a Statham strain gage and recorded
as described.
In some cases a small polyethylene tube was
passed into the pleural space through the lumen of a
blunt 15-gage needle. "Effective" pressure within
the left ventricle was calculated by subtracting the
intrapleural pressure from the intraventricular
pressure. Femoral arterial pressure was measured
with a strain gage and recorded as described above.
The areas of pressure curves were obtained by means
of a planimeter. Stroke work was calculated in the
usual manner using the average of left ventricular
systolic pressure and femoral diastolic pressure.
In some experiments, several determinations of
effective intraventricular pressure and EDV were
made at 5 or 10 min. intervals. Following this,
plethora was induced by means of rapidly infusing
into the femoral vein, in a period of approximately 5
min., a large volume of blood from a donor dog.
Immediately following this, several determinations
of effective ventricular pressure and EDV were
made at approximately 5 min. intervals. In another
series of experiments a state of plethora was induced
by infusing a mixture of the dog's blood with 5
per cent dextran*-saline solution in an amount equal
to 8 per cent of the dog's body weight. This blooddextran mixture was prepared by infusing a 5 per
cent dextran-saline solution into the dog in an
amount equal to 2?s per cent of the dog's body
weight and allowing the dextran solution to mix with
the. clog's blood in vivo. A few minutes later the dog
was bled an amount equal to the injected solution.
This procedure was carried out three times until all
of the dextran solution had been mixed with the
dog's blood in vivo. This gave a total amount of withdrawn blood-dextran mixture equal to S per cent
of the dog's body weight. Plethora was then induced
by infusing all of this blood-dextran mixture into
the animal at one time. It was desirable to induce
plethora in this manner, because a change in the
per cent of plasma in the blood produces a change
in the calibration factor of the electric conductivity
measurement used in determining the EDV. Because
of the. large volume of dextran solution infused, the
average per cent concentration of plasma in the
blood was quite high in all experiments, the average
being 78.5 per cent plasma. Before and immediately
following the infusion of the blood-dextran solution
the EDV, ESV, stroke volume and pressure determinations were repeated several times; the animal
* Kindly supplied by the Commercial Solvents
Corporation.
was then bled approximately 250 ml. and the determinations repeated several times. The bleedings
were repeated, carrying out two or more determinations of EDV, and effective intraventricular pressure
after each determination, until the animal was bled
to death.
RESULTS
Relationship Between EDV and End-Diastolic
Ventricular Pressure. We have carried out 154
simultaneous determinations of "effective"
end-diastolic pressure (EEDP) or intraventricular end-diastolic pressure (EDP) and
EDV in 12 dogs. In 3 dogs left ventricular
EDV determinations were made in the control
state and after infusing several hundred milliliters of blood from a donor dog. In 9 dogs the
studies were carried out in the control state,
after infusing a dextran-blood mixture in an
amount equal to 8 per cent of the body weight,
and after each of several hemorrhages until
the animal was bled to death. Examples of the
results in individual animals are given in
figures \A, B, C. Each figure gives the results
of all the determinations on an individual
animal. In figure 1/1, it is seen that although
the EDV changed greatly there was no consistent change in EDP; there were random
variations but it remained constant, or increased slightly, even though the EDV changed
several fold. In figure IB, it is seen that with
the smallest EDV consistent with life, EEDP
was the same or slightly less than it was when
the EDV was several times larger. After a
certain large EDV was reached EEDP increased greatly with no consistent change in
EDV. In figure \C, it will be noted that as the
EDV increased several fold from its lowest
value up to a certain point, there was some
increase in EEDP; beyond this point there
was no consistent change in EDV although
EEDP increased greatly. In all animals studied,
beginning with the smallest EDV consistent
with life, there was either no change or a
slight increase in EEDP or EDP while the
EDV increased several fold; in 8 of 12 animals
studied, after a certain large value of EDV
was reached, a further small increase in EDV
was associated with a very large increase in
EEDP or EDP.
It will be noted in figure \C, that immedi-
275
HOLT
One Dog
60
H
One Dog
1
1
H-
X
E 40
Q.
Q
20
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0
I
OneDog
40
E
a.
20
Q
H.O
t-0.5
N
-0.5
-1.0'0
20
40
60
80
100
120
140
EDV(ml.)
160
10 20
30 40
50 60
70
EDV(ml.)
FIG. 1. /I, B, C, D. Relationships between end-diastolic (EDP) effective end-diastolic (EEDP)
pressures and blood volume as ordinates to end-diastolic volume (EDV) as abscissa under conditions described. E, F, G, H. Relationships of end-systolic volume (ESV), stroke volume, pressure
and stroke work as ordinates to end-diastolic volume (EDV) as abscissa under conditions described.
ately following the infusion (point 1) the EEDP
was at its highest value (41 mm. Hg) and this
was associated with an EDV of 79 ml., while
20 min. later and after bleeding 300 ml. of
blood (point 4) the EEDP was lower (16 mm.
Hg) but the EDV was larger, namely 112 ml.
Results similar to this were obtained in 10 of
12 dogs. Although the reason is not well understood a possible explanation is that, immediately following the infusion into the venous
system, the right ventricle is greatly distended
under a high pressure and because of the relatively inelastic pericardium the right ventricle
imposes on the left and prevents the left
ventricle from increasing further in volume;
after .15 or 20 min., or after hemorrhage, a
redistribution of blood takes place with the
right ventricle decreasing in volume, thus
allowing the left ventricle to increase its EDV.
Relationship Between EDV and Blood Volume.
Although the blood volume was not measured
in these experiments the relative blood volume
was estimated to be the control blood volume
plus the amount of fluid infused or minus the
amount hemorrhaged. Results similar to those
shown in figure ID, were obtained in 8 of 9
experiments. It is seen that as the estimated
blood volume decreased the end-diastolic
volume decreased.
Relationship Between EDV and ESV. The
results of a typical experiment are shown in
figure IE. As the EDV increased the ESV
27G PLETHORA AND HEMORRHAGE OX LEFT VENTRICULAR VOLUME AX I) PRESSURE
Relationship Between EDV and Systolic
Pressure, Diastolic Pressure, and. Pulse Pressure.
The results of a typical experiment showing
ESV = 0.V2EDV - 0.43
the relationship between left ventricular
systolic pressure and EDV in one animal are
The standard deviation of ESV from the
shown in figure .1(7. It will be noted that as
regression of ESV on EDV in this experiment
the EDV increased from a minimal value there
was ±2.5 ml. The equations of the lines, in
was an increase in systolic pressure; after a
the 12 dogs studied, calculated by the method
certain large value of EDV was reached
of least squares with the standard deviation of
further
increase in EDV was associated with no
ESV from the regression of ESV on EDV are
consistent
change in systolic pressure. Results
given in table 1.
similar
to
these
were obtained in all 12 dogs.
Relationship Between ED V and Stroke Volume
Similar
results
were obtained for femoral
(S). The results of a typical experiment are
diastolic
pressure
and femoral pulse pressure,
shown in figure l/<\ As the EDV increased the
as
well
as
for
total
femoral arterial pressure
stroke volume increased in a linear fashion
area
per
heart
beat.
having the equation:
Relationship Between EDV and, Stroke Work.
S = 0.38 EDV + 0.38
The results of a typical experiment are shown
The standard deviation of the stroke, <S, from
in figure Iff. As the EDV increased the stroke
the regression of the stroke on EDV in this
work increased until a certain large value for
experiment was ±2.4 ml. The equation of the
stroke work was reached, beyond this point
lines, in all dogs studied is given in table 1.
further increase in EDV was associated with
little or no increase in stroke work. Results
similar to this were obtained in all but a few
TABLE 1.—Results of Experiments Shoxoinij a Linear
Relationship Between ESV and EDV, and Stroke
dogs, and in these dogs the stroke work conVolume and EDV
tinued to increase over the entire range of the
end-diastolic
volumes and the point was not
Equation
Equation
DOR
ESV --= m(EDV) + b
S = m(EDV) + b
reached where stroke work remained constant
but the end-diastolic volume continued to
in
b
s
b
m
5"
*
(K-K.)
(±)
(±)
increase.
Relationship Between ES\' and, "Effective"
4.5 0.50 -15.2
2
10.9 0.50 16.0
4.5
3.7 0.29
20.0 0.73 - 5 . 9
5.1 3.S
3
End-Diastolic Pressure. There was no con4
27.1 0.S4 - 9 . 5
4.3 0.15
10.1 4.3
sistent relationship between "effective" end
16.7 0.62
1.5
10.5 0.36 - 0 . 3 9.4
0
diastolic pressure and ESV, there being con6.2
10
15.5 0.51
3.9 0.49 - 6 . 2 2.9
siderable scatter of the data.
11
5.1 0.67 -10.2
5.4
16.5 0.32 10.0
16.3 0.64
12
4.5 0.37 -6.S
Relationship Between Ventricular Residual
5.5
5.0
- 0 . 2 5.7
5.7 0.42
.18.7 0.57
13
1.5
Fraction and Blood, Volume. The results ob18.0 0.71 - 3 . 3
3.0
5.7 0.30
14
5.7
tained in one dog are shown in figure 2/1.
13.2 0.47
2.1
2.9 0.52
-2.S 2.S
15
As
the blood volume increased the fraction of
2.2 2.2
0.35
6.9
20.9 0.64 -2.4
16
the
EDV retained at the end of each beat
0.4 2.4
17
14.8 0.62 -0.4
2.5 0.38
(Cn/C-i) decreased. Results similar to this were
Avgs. 18.2 0.60 + 1.0 +5.0 0.40 -1.7 ±4.5
obtained in 10 of 12 dogs.
Relationship Between Ventricular Residual
Under the equation of the line relating ESV and
Fraction
and Systolic Pressure, Diastolic PresEDV are listed for each experiment the values of the
sure, and Pulse Pressure. The results of a typical
slope of the line, m, the intercept of the line, b, on
the ESV axis and the standard deviation, s, of ESV
experiment on one animal are shown in figure
from the regression of ESV on EDV. The data relatIB. It will be noted that as the ventricular
ing stroke volume, S, to EDV is treated in a similar
systolic
pressure increased the fraction of the
manner. In all of the above equations EDV, ESV,
EDV
retained
at the end of each beat decreased.
and stroke volume are expressed in ml. See text for
further discussion.
Results similar to this were obtained in 11 of
increased in a linear fashion having the equation :
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HOLT
277
+ 2.0
One Dog
a> +1.0
E
Blood Voh
3
N
-1.0
-2.0
-+•
One Dog
X
E
150
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100
50
0.2
0.4
0.6
0.8
1.0
Residual Fraction
FIG. 2. A . Relationship between estimated blood
volume and loft ventricular residual fraction. The
residual fraction, average value of C,,/Cn-t, obtained
in each electric conductivity determination. A',
Control animal. H. Relationship between left ventricular peak systolic pressure and residual fraction.
12 dogs. Similar results were obtained when
0,,/C-i was plotted against femoral diastolic
pressure and femoral pulse pressure in most of
the animals studied.
Relationship Between Ventricular Residual
Fraction and Stroke Work. As the stroke work
increased the residual fraction decreased. Jn
G of 12 experiments the relationship appeared
to be linear while in the remaining half of the
experiments there was considerable scatter of
the data.
Relationship Between Stroke Work and
"Effective" I'Jnd-Diastolic Pressure. The results
of a typical experiment are shown in figure
3/1. It will be noted that as the stroke work
increased several fold from a low value there
was a small increase in the EED.P; after a
certain value of EKJDP was reached further
increase of EISDP was associated with a small
increase or no change in stroke work. Results
similar to this were obtained in 4 of 7 dogs;
in the remaining 3 of the 7 dogs a small increase in EEDP was associated with a large
increase in stroke work, and the point was not
reached where a further increase in EEDP
0
20
40
60
80
100
Stroke Work (gram.)
FJG. 3. A. Relationship between stroke work
and left ventricular "effective" end-diastolic pressure, li. Relationship between loft ventricular peak
systolic pressure and stroke work. C. Relationship
between planimetered femoral arterial pulse pressure area and stroke work. Xote the approximately
linear relationship. Equation of the line is shown in
the figure. W, Stroke work.
was associated with little or no change in
stroke work.
Relationship Between Stroke Work and
Systolic Pressure, Diastolic Pressure, and Mean
Arterial Pressure. As the stroke work increased
the systolic pressure increased as shown in
figure 3B. Results similar to this were obtained
in all 12 experiments. A similar relationship
278
PLETHORA AND HEMORRHAGE OX LEFT VENTRICULAR VOLUME AND PRESSURE
250
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20
30
Stroke (ml.)
FIG. 4. Relationship between left ventricular
peak systolic pressure and stroke volume. Note that
as the stroke volume increases the pressure increases
but after a certain large pressure is reached further
increase in stroke volume is associated with little
or no increase in pressure.
was found between stroke work and mean
arterial pressure and diastolic pressure. When
the data in figure 3B was plotted on semi-log
paper, with the stroke work plotted on the
logarithmic scale and the systolic pressure
plotted on the linear scale, there appeared to
be a linear relationship between the log of the
stroke work and the systolic pressure.
Relationship Between Stroke Work and
Planimetered Pulse Pressure Area -per Beat.
As the stroke work increased the pulse area
per beat increased in a linear fashion, as shown
in figure 3C. Results similar to this were obtained in 11 of 12 experiments.
Relationship Between Stroke Volume and
Systolic Pressure, Diastolic Pressure, and Pulse
Pressure. The results of a typical experiment
in one dog are shown in figure 4. It will be
noted that as the stroke volume increased the
left ventricular systolic pressure increased
markedly; after a certain large value for stroke
volume was reached further increase in stroke
volume was associated with little or no increase
in systolic pressure. Results similar to this were
obtained in all 12 dogs. Similar results were
obtained in most experiments when stroke
volume was plotted against femoral diastolic
pressure and femoral pulse pressure.
DISCUSSION
It is clear, I believe, from the results obtained when the EDV and the EEDP or
EDP were measured simultaneously in an
animal subjected to plethora and hemorrhage,
that the EDV may vary over a wide range
with either no change or a slight increase in
the EEDP distending the ventricle. It would
appear from these results that up to a point
the left ventricle behaves as a flaccid bag and
that its volume may change with little or no
change in its distending pressure. This view is
supported to some degree by the results obtained by Rushmer and Thai6 which show no
consistent relationship between effective filling
pressure and cross section of the left ventricle
in diastole. After a certain large volume is
reached the ventricle appears no longer to
behave as a flaccid bag, but behaves as if its
walls were more or less rigid; and therefore
the EDV remains constant even though the
distending pressure increases greatly. Under
these circumstances one or more of the following may have occurred: (1) The tone of the
left ventricular muscle may have increased;
(2) the ventricular muscle may have been
stretched to its elastic limit; (3) the ventricle
and other chambers of the heart may have
increased to the point where the inelastic
pericardial membrane supported the ventricular walls in such a manner that they behaved
as if they were rigid; (4) the right ventricle may
in some way have affected the volume of the
left ventricle.
That the ventricle was not stretched to its
elastic limit is suggested by the earlier work
of Evans and Matsuoka7 and Kunos on the
heart-lung preparation. The view that the
pericardium may restrict the ventricles from
expanding beyond a certain point is supported
by the recent work of Berglund and co-workers9
who have presented evidence that in the openchest dog when the left ventricle was stressed
and caused to dilate, the right, ventricle function curve was lowered. Removal of the pericardium abolished this effect of the left ventricle on the right ventricle. The fact that
immediately following infusion the EEDP
was high but the EDV was small compared to
the EDV a short time later (or after a small
279
HOLT
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hemorrhage) when it was lower, suggests that
either the tone of the left ventricle changed or
the right ventricle in some way affected the
EDV of the left ventricle. Further experiments
are necessary to clarify this matter. In particular, it is desirable to cany out similar studies
on animals before and after removal of the
pericardium, in order to ascertain the role
played by the pericardium; and to carry out
studies similar to those described here on the
right ventricle and simultaneously on both
ventricles. Since the right and left atria, as
well as the right and left ventricles, are contained within the pericardium, consideration
must be given to what effect the atria have on
the ventricular volumes and pressures.
The data on estimated blood volume, EDV,
ESV, and stroke volume indicate that as blood
volume increases the EDV, ESV, and stroke
volume increase, and as blood volume decreases these factors decrease. It is desirable
that studies be carried out in which blood volume is accurately measured simultaneously
with the determination of EDV, ESV, and
stroke volume. The fact that the EDV, stroke
volume, and stroke work may vary over a
wide range with either no increase or a slight
increase in EEDP and that after a certain
large EDV, stroke volume or stroke work is
reached there may be large variations in EEDP
with little change in EDV, stroke volume or
stroke work indicates that in the closed-chest
dog neither the useful work nor the energy of
myocardial contraction are related to the
EEDP. This view is given further support by
the fact that in 10 out of 12 experiments
immediately following the development of
plethora the EEDP or EDP was higher than it
was 15 or 20 min. later, but the EDV immediately following the development of plethora
was smaller than it was 15 or 20 min. later
when the EEDP was lower.
Our results which show that the stroke
work may vary over a wide range with only
a small increase in EEDP and that after a
certain large stroke work is reached there may
be large variations in EEDP with little change
in stroke work are in general agreement with
the results obtained by Sarnoff and Berglund6
in (he open-chest dog, except that in their
experiments the increase in stroke work,
beginning with the smallest stroke work, was
at times associated with a greater increase in
left ventricular distending pressure; and our
data differs to some degree from the data of
Ullrich and Kramer10 on the pressure-volume
curves of the left ventricle in the open-chest
dog which show that for a given increase in
EDV, beginning with the smallest EDV, there
is generally a considerable increase in left
intraventricular pressure. The reason for the
small difference between our data and that of
the above workers is not perfectly clear, but it
may well be that the difference is due to the
fact that our experiments were carried out in
the closed-chest dog, while theirs were carried
out in the open-chest dog. This view is given
support by the fact that in the studies of
Berglund,11 relating stroke work to "effective"
mean left atrial pressure in the dog after closure
of the chest and with the pericardium intact,
the results obtained were similar to those of
our experiments. It may well be that the functioning of the left ventricle differs in the openchest animal from that of the closed-chest
animal.
The fact that there is a decrease in the
fraction of the EDV that is retained by the
ventricle with each stroke as the blood volume,
systolic pressure, diastolic pressure, pulse
pressure, stroke work, stroke volume, and
ESV increase is explained by the fact that the
ventricle is never able to completely empty
itself, and the fact that as the EDV increases
the ESV increases. For after a severe hemorrhage the EDV and stroke volume are small,
and since a certain minimum ESV is always
retained by the ventricle, the fraction of the
EDV retained by the ventricle at the end of
systole is large after hemorrhage; while when
the EDV is large, the ESV and stroke volume
are large and the fraction of the EDV retained
after each stroke is small.
SUMMARY
In the anesthetized closed-chest animal the
effects of plethora and hemorrhage on the
end-diastolic volume (EDV), end systolic
volume (ESV), stroke volume and other
circulatory factors were studied. Increase in
280
'LKTHORA AND HKMORRHAGE OX LEFT VENTRICULAR VOLUME AND PRESSURE
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blood volume resulted in an increase in enddiastolie volume, end-systolic volume, stroke
volume, stroke work, and arterial pressure, and
a decrease in the traction of the end-diastolic
volume retained at the end of systole. A decrease in blood volume had the opposite
effect. It was shown that there was little
change, or a slight increase, in "effective"
end-diastolic pressure when the end-diastolic
volume increased several fold, beginning with
the smallest end-diastolie volume consistent
with life. After a certain large value of enddiastolic volume was reached the "effective"
end-diastolic pressure increased greatly with
little or no change in end-diastolic volume.
Equations showing the linear relationship
between end-diastolic volume and end-systolic
volume and between end-diastolic volume and
stroke volume are given.
vite e que, post ciue un certe alte valor del volumine termino-diastolic esseva attingite, le
"effective" pression termino-diastolic se augmentava grandemente con pane o nulle alteration in le volumine termino-diastolic. Es presentate equationes que demonstra le relation
linear inter le volumine termino-diastolic e le
volumine termino-systolic e inter le volumine
termino-diastolic e le volumine per pulso.
1
2
I am indebted to Dr. 0. \V. Shadle for his participation in the measurement of the pressure in many
of these experiments.
SUMMAUK) IX IXTEHLINGUA
in anesthesiate animates a thorace clauditc,
le elTectos esseva studiate c[lie plethora e hemorrhagia exerce super le volumine terminodiastolie, le volumine termino-systolic, le volumine pulsatile, e altere factores circulatori.
Augmento de volumine sanguinee resultava in
un augmento del volumine termino-diastolic,
del volumine termino-systolic, del volumine per
pulso, del labor pulsatile, e del pression arterial
e in un reduction del fraction del volumine
termino-diastolic que es retenite al tin del
systole. Un reduction del volumine de sanguine
habeva le effecto contrari. Esseva monstrate
que il occurreva pane alteration o leve grados
de augmento in le "effective" pression terminodiastolic quando le volumine termino-diastolic
esseva augmentate per plure vices le plus basse
valor initial sufh'cientc pro le mantenentia de
PATTERSON, S. \V., PIPER, If.,
AND STARLING,
I'J. H.: The regulation of the heart beat. .1.
Physiol. 48: 465, 1914.
3
HAMILTON, W. F.: The Lewis A. Connor Memorial
Lecture: The physiology of the cardiac output.
Circulation 8: 527, 1953.
4
ACKNOWLEDGMENT
REFERKXCI'K
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Effect of Plethora and Hemorrhage on Left Ventricular Volume and Pressure
J. P. HOLT, J. Allensworth, J. Diana, David Collins and Helga Kines
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Circ Res. 1957;5:273-280
doi: 10.1161/01.RES.5.3.273
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