Vol. 274, Issue 1, H187-H192, January 1998
Impairment of contraction increases sensitivity of epicardial
lymph pressure for left ventricular pressure
Jurgen W. G. E.
Vanteeffelen,
Daphne
Merkus,
Luc J.
Bos,
Isabelle
Vergroesen, and
Jos A. E.
Spaan
Department of Medical Physics, Academic Medical Center,
University of Amsterdam, 1100 DE Amsterdam, The Netherlands
 |
ABSTRACT |
In the present study, cardiac contraction was
regionally impaired to investigate the relationship between
contractility [maximum first time derivative of left ventricular
pressure
(dPLV/dtmax)] and PLV on epicardial lymph
pressure (Plymph) generation.
Measurements were performed in open-chest anesthetized dogs under
control conditions and while local contraction was abolished by
intracoronary administration of lidocaine. Lidocaine significantly
lowered
dPLV/dtmax
and PLV pulse to 77 ± 9 (SD;
n = 5) and 82 ± 5% of control,
respectively, whereas Plymph pulse
increased to 186 ± 101%. The relative increase of maximum
Plymph to
PLV related inversely to the
change in
dPLV/dtmax after lidocaine administration. Additional data were obtained when
PLV was transiently increased by
constriction of the descending aorta. The ratio of pulse
Plymph to
PLV during aortic clamping increased after lidocaine administration, from 0.063 ± 0.03 to 0.15 ± 0.09. The results suggest that transmission of
PLV to the cardiac lymphatic
vasculature is enhanced when regional contraction is impaired. These
findings imply that during normal, unimpaired contraction lymph vessels
are shielded from high systolic
PLV by the myocardium itself.
lidocaine; contractility; left ventricular pressure transmission; myocardial edema
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INTRODUCTION |
EPICARDIAL LYMPH PRESSURE
(Plymph) measurements can
provide instantaneous information on changes in forces that are
involved in regulation of the myocardial interstitial fluid balance
(13). The generation of lymph pressure is assumed to be brought about by an interplay of the varying stiffness of the cardiac muscle surrounding the lymphatics and transmission of left ventricular pressure (PLV) (3, 4, 11). The
sensitivity of lymph pressure for
PLV was found by Han et al. (3) to
be 10 times higher in diastole than in systole. From this finding and
that of Kouwenhoven et al. (6), who found that coronary inflow was
affected by PLV in early systole
but not in midsystole during constant pressure perfusion of the left
main coronary artery, it has been hypothesized that the transmission of
PLV to the intramyocardial blood
and lymph vessels depends on the contractile state of the myocardium (3, 6, 11). It has been suggested that during systole the
intramyocardial vessels are shielded from
PLV transmission by the increasing
elastance of the myocardium (2, 6, 11). This mechanism is thought to
protect the vessels from collapse during cardiac contraction.
The shielding effect might be diminished during regional impairment of
cardiac contraction, when local force generation is uncoupled from
PLV. In the present study, the
effect of regional impairment of cardiac contraction on
Plymph generation was
investigated. Measurements were performed in open-chest, anesthetized
dogs during control conditions and while local contraction was
abolished by intracoronary administration of lidocaine in a distal
portion of the left anterior descending artery (LAD) (2, 5, 8). In both
conditions the sensitivity of lymph pressure for a change in
PLV was investigated.
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METHODS |
Experimental preparation and measurements.
Six mongrel dogs of either sex, weighing 20-30 kg, were
premedicated by intramuscular injection of 1 ml of methadone and 1.5 ml
of xylazine (20 mg/ml; Rompun, Bayer, Leverkusen, Germany). General
anesthesia was induced by intravenous injection of 4 ml of
pentobarbital sodium (60 mg/ml). After tracheal intubation, the animals
were ventilated with a Harvard respirator using a 2:1 nitrous
oxide-oxygen mixture. Anesthesia was maintained by 40 ml fentanyl (0.05 mg/ml in 10 min). Arterial blood gases and pH were measured frequently,
and to keep them within the physiological range ventilator settings
were adjusted. Depth of anesthesia was assessed by changes in heart
rate, blood pressure, and reflexes, and anesthetics were administered
when necessary.
A left thoracotomy was performed in the fifth intercostal space, and
the heart was exposed and suspended in a pericardial cradle. A
fluid-filled polyethylene catheter was placed into the ascending aorta
via the carotid artery and connected to a dome pressure transducer
(Bell and Howell 4-327I) for aortic pressure (PAo) monitoring. Umbilical tape
was placed around the descending aorta to form a snare. A catheter tip
manometer (5 F, Millar SPC-350) was inserted through a purse string in
the apex into the left ventricle for the measurement of
PLV. The middle portion of the LAD
was dissected free, and a 2-mm perivascular transit-time flow transducer (2SB) was placed around it and connected to a Transonics T206-S flowmeter (Transonics Systems, Ithaca, NY) for measurement of
LAD flow
(
LAD).
Distal from the flow transducer, a Venflon 2 IV cannula (22G,0.8-mm OD)
was introduced through the wall of the LAD and connected with a
three-way stopcock to a fluid-filled polyethylene catheter. Coronary
arterial pressure was measured by connecting this catheter to a dome
pressure transducer.
An epicardial lymph vessel on the distal anterior wall of the left
ventricle was cannulated retrogradely with a heparinized polyethylene
cannula (PE-90, OD 0.96 mm, ID 0.58 mm), as described elsewhere (3, 4).
After cannulation of the lymph vessel, the cannula slowly filled with
lymph fluid. When the cannula was completely filled, a microtip
pressure transducer with a lumen (5 Fr, Philips) was connected to the
cannula via a homemade Perspex connector (4). Air in the connector and
the lumen was removed by flushing with saline. During measurements the
lumen of the pressure transducer was closed, thereby obstructing the
lymph flow. In this way Plymph
increased to a steady-state level. If mean
Plymph did not increase or the
cannula was not filled spontaneously with lymph fluid, the lymph
cannulation was considered unsuccessful. The lumen of the microtip
pressure transducer was regularly opened to prevent possible artifacts
because of a prolonged obstruction of the lymph flow.
Zero pressures were set at midchest level. The zero flow of the
flowmeter was obtained by a short occlusion of the LAD several times
during the experiment. Signals were digitized on-line during relevant
interventions at a sample rate of 80 Hz and subsequently were stored on
hard disk for off-line signal analysis.
Protocol.
Steady-state conditions were achieved. During these control conditions,
PLV was varied repeatedly by
constriction of the descending aorta for several beats. Subsequently,
we tried to abolish contractility in the region of the cannulated lymph
vessel by injecting 1 ml of 1% lidocaine via the three-way stopcock
into the LAD. Local abolishment of contractility was assessed by
epicardial imaging of cardiac functioning with an echo apparatus (5 MHz; 77020-series ultrasound system, Hewlett-Packard). In general,
~20 s after lidocaine administration, echo demonstrated regional lack
of contraction in the area perfused by the LAD. This part of the left
ventricular free wall was passively deformed during the cardiac cycle
by the contracting part of the ventricle on the one hand and
PLV on the other hand. The effect
persisted for several minutes. During this period of regional
impairment of cardiac contraction, the descending aorta was again
regularly constricted. When 1 ml of 1% lidocaine did not have a clear
effect, a larger volume (2-3 ml) of lidocaine was injected. We
attempted to repeat lidocaine injection several times in each
experiment.
It should be noted that the placement of the ultrasound transducer
formed a risk for the stability of the lymph cannula and also
influenced the Plymph measurement
by slight compression of the tissue. Therefore, quantitative
measurements were not made from the images. Echo was only used to judge
whether the lidocaine injection was effective in diminishing local
contractility.
Data analysis.
The first time derivative of PLV
(dPLV/dt)
was calculated and its maximum
(dPLV/dtmax)
was taken as a measure of contractility. Pulsatility of flow and
pressure was defined as the difference between the minimum and the
maximum per beat. The sensitivity of
Plymph to
PLV was analyzed by determining
the ratio in pulse pressure of
Plymph to
PLV for 15-50 beats during
the periods in which PLV was
varied in each animal. Furthermore, linear regression analysis was
performed on the relationship between the pulse pressures of
PLV and
Plymph. To verify whether linear
regression analysis was allowed, residuals of all individual
regressions were tested for independence.
Data were analyzed for both the control period and the period in which
cardiac contraction was impaired, as indicated by a decrease in
dPLV/dtmax.
Data of all animals were averaged and are presented as means ± SD.
Differences induced by the impairment of cardiac contraction were
tested by a paired Student's t-test (one-sided). P < 0.05 was considered
significant.
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RESULTS |
Effects of lidocaine.
In Fig. 1 tracings of
LAD,
PAo,
Plymph,
PLV, and
dPLV/dt
from one experiment before and after the injection of lidocaine are
shown. After the start of lidocaine injection,
dPLV/dtmax decreased within a few beats from 1,274 to 997 mmHg/s and
PLV pulse decreased from 72.4 to
69.6 mmHg. After an initial small decrease for about five beats during
the injection of lidocaine, pulse
Plymph increased to 23.3 mmHg
within ~20 s.
LAD pulsatility decreased, and systolic backflow was diminished after the injection of
lidocaine.
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Fig. 1.
Effect of lidocaine administration on left anterior descending artery
flow (LAD),
aortic pressure (PAo),
epicardial lymph pressure
(Plymph), left ventricular
pressure (PLV), and first time
derivative of PLV
(dPLV/dt).
Left, control tracings;
right, tracings during impaired
regional contraction. Arrow shows start of injection of lidocaine as
indicated by change in
LAD.
Administration of lidocaine results in a decrease in
dPLV/dtmax,
indicating impairment of LV function. Pulsatility of
PLV and
LAD is decreased
during impaired contraction, whereas
Plymph pulsatility is increased.
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Average data are presented in Table 1.
Average
dPLV/dtmax
decreased from 1,447 ± 173 to 1,102 ± 150 mmHg/s
(P < 0.05) after the administration
of lidocaine. Although pulse PLV
decreased from 102 to 84 mmHg, pulse
Plymph increased on average from
6.2 to 12.2 mmHg. After lidocaine, heart rate increased on average from
106 to 119 beats/min (P < 0.05).
In one animal, diastolic Plymph
increased from a control value of 19.6 mmHg to a value of 84.3 mmHg
after lidocaine injection, although pulsatility did not change. This
behavior is considered typical for the presence of intraluminal
lymphatic valves. Therefore, this animal was excluded from the overall
analysis.
After cessation of infusion of lidocaine, cardiac contraction remained
diminished for several minutes. The affected ventricular region then
gradually recovered, and Plymph
and PLV returned to their control
values at a comparable rate. The ratio of maximum Plymph over maximum
PLV per beat was calculated for
several beats in the period after the injection of lidocaine. In this
way, measurements of
Plymph/PLV
were obtained at different values of
dPLV/dtmax, reflecting varying degrees of regional impairment of cardiac
contraction. In Fig. 2 the relationship
between
Plymph/PLV
and
dPLV/dtmax
after the administration of lidocaine is shown for all animals. In each animal
Plymph/PLV
was inversely related to
dPLV/dtmax.
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Fig. 2.
Relation between
dPLV/dtmax
and ratio of maximum per beat of
Plymph over
PLV for all experiments
(n = 5 animals). Data are normalized
to control values, i.e., before injection of lidocaine. Each individual
animal is depicted by a different symbol;  , control value for all
animals. Different values of
dPLV/dtmax,
representing different contractile states, were obtained after
lidocaine administration as affected region gradually recovered. Each
data point represents average value of 30-100 beats. Linear fits
(dashed lines) are depicted for each animal for clarity. In each
animal, sensitivity of Plymph for
PLV was inversely related to
dPLV/dtmax
after lidocaine injection.
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Effect of PLV on
Plymph.
In Fig. 3 the effect of aortic
clamping on LAD,
PAo, Plymph, and PLV
is demonstrated during control conditions and during regional
impairment of cardiac contraction with lidocaine. Constriction of the
descending aorta increased PLV
and, concomitantly, PAo and
LAD.
Furthermore, a small increase in
Plymph could be detected during
control. Administration of lidocaine distinctly intensified the
increase in Plymph during aortic
clamping. In this experiment Plymph pulse increased from 2.9 to
4.8 mmHg during the fourth beat of aortic clamping in
control, whereas with lidocaine the pulse increased from 4.1 to
10.6 mmHg.
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Fig. 3.
Effect of aortic clamping on
LAD,
PAo,
Plymph, and
PLV control
(left) and after lidocaine
administration (right). Constriction
of descending aorta results in an increase in
PLV,
PAo,
LAD, and
Plymph. Effect on
Plymph is distinctly enhanced
after lidocaine injection. Note that in contrast to results shown in
Fig. 1 and Table 1, diastolic
Plymph was lower during regionally
impaired contraction in this experiment.
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The overall relationship between pulse pressure of
PLV and
Plymph in this animal before and
after administration of lidocaine is shown in Fig.
4. Linear regression analysis revealed that
the slope between both variables increased from 0.044 ± 0.006 during control to 0.20 ± 0.023 when cardiac contraction was
diminished, indicating that the sensitivity of
Plymph for
PLV increased during regionally
impaired contraction.
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Fig. 4.
Example of relationship between pulse pressure of
PLV and
Plymph during unimpaired (control)
and impaired (lidocaine) cardiac contraction. Relationship between
pulse PLV and
Plymph in this animal is given by
Plymph = 0.044 · PLV  3.1 during control conditions and by
Plymph = 0.21 · PLV 20.8 after lidocaine administration. Sensitivity of
Plymph for
PLV is increased after lidocaine
administration.
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Average data on the relationship between pulse
PLV and
Plymph are presented in Table
2. Lidocaine increased the slope of the
relationship between pulse pressure of
PLV and
Plymph. After lidocaine injection
the sensitivity of pulse pressure in
Plymph to
PLV increased from an average of
6.3% to 15%.
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Table 2.
Linear regression coefficients for relationship between pulse
PLV and pulse Plymph during aortic clamping
before and after lidocaine
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DISCUSSION |
In the present study epicardial lymph pressure generation was studied
in a region of left ventricular myocardium during normal contraction
and while contraction in that region was impaired with lidocaine. The
main finding of the study is that regional impairment of contraction
results in an increased sensitivity of lymph pressure for a change in
left ventricular pressure. The sensitivity of lymph pressure for left
ventricular cavity pressure after lidocaine injection was about two
times higher than in control, and the sensitivity was demonstrated to
be inversely related to dPLV/dtmax.
These findings indicate that the transmission of left ventricular
pressure to the lymphatic vasculature is related to the contractile
state of the myocardium.
Experimental limitations.
To diminish contractility of a part of the left ventricle, lidocaine
was injected in the middle portion of the LAD and the intended result
on heart contraction was judged by means of echo. Echo images revealed
that after lidocaine injection a delimited portion of the left
ventricular free wall did not take part in the wall thickening process
during systole but was passively deformed instead. Because of
interference of the echo transducer with the lymph cannula, as
indicated in METHODS, wall thickness
could not be determined continuously by echo. In addition to the echo
measurements, dPLV/dtmax
was calculated to determine the effect of lidocaine on regional
myocardial contractility. As shown in Fig. 1,
dPLV/dtmax immediately decreased after the lidocaine injection was started. The
decrease is in agreement with the proposed role for lidocaine to
diminish cardiac contractility.
Lidocaine has been widely used in experimental studies for its negative
inotropic properties (2, 5, 8). Doucette et al. (2) measured regional
myocardial thickening fraction by a Doppler ultrasonic probe and
demonstrated that in contrast to normal contraction, in which wall
thickening occurs during systole, injection of 1 ml of 4% lidocaine
into the LAD resulted in a rapid thinning of the wall at the onset of
systole, which was completed by the end of isovolumic systole. During
the ejection phase of systole no further thinning was observed.
Although the concentration of lidocaine used in their study was
somewhat higher than that in our study, it is likely that the observed
effect on local contraction is similar. Indeed, the maximum decrease in
dPLV/dtmax
in the present study caused by the administration of lidocaine was
comparable to the decrease found by Doucette et al. (2). Marzilli et
al. (8) also found an absence of systolic thickening after infusion of
lidocaine into the LAD for several minutes.
It might be suggested that the increase in lymph pressure after the
lidocaine injection results from a direct effect of lidocaine on the
lymph vessels, i.e., depression of the intrinsic contractility of the
lymph vessels. Although lymph vessels do possess some intrinsic contractility, it is not very likely that this factor is involved in
the generation of lymph pressure in the heart because of the dominant
role of cardiac contraction in the pressure generation. This is
demonstrated by the lymph pressure waveform shown in Fig. 1: major
pulsations in lymph pressure appear at a frequency equal to the heart
rate.
In the current study it was observed that impaired contraction reduced
mean and diastolic arterial flow. Furthermore, pulsatility of arterial
flow was decreased as well. This latter finding appears to contrast
with the findings of Doucette et al. (2), who found a large increase in
the amplitude of distal flow velocity, whereas proximal coronary flow
did not change. It should be noted that in their study the coronary bed
was maximally dilated by adenosine while mean coronary perfusion
pressure was held constant by means of a perfusion system. In our
experiments, however, aortic pressure acted as perfusion pressure for
the coronary bed, and its reduction after lidocaine administration may
have decreased coronary arterial flow. Furthermore, because coronary
tone was not abolished in our experiments, vasoconstriction in response
to a decrease in metabolism after lidocaine may also have contributed
to the decreased coronary flow pulsatility.
Interpretation of experimental findings.
The increase in Plymph after the
administration of lidocaine is likely to be explained by an increased
transmission of PLV to the lymph
vessels. As indicated by the doubling of the ratio of pulse
Plymph to
PLV during aortic clamping (Table
2), Plymph was more sensitive to
changes in PLV during diminished
contraction compared with control. It might be suggested that the
increase in Plymph during
lidocaine and the increased sensitivity for
PLV are related to deformation of
the embedded lymph vessels by stretching of the noncontracting region
during systole. Although it is very well possible that the myocardial
lymph vasculature is affected by this mechanism, it is not obvious that
it would result in an increase in
Plymph per se. Our pressure
measurement reflects Plymph further upstream, inside the myocardium. The measured
Plymph is determined by the
pressure generated by a particular pressure source inside the
myocardium and the resistance distribution proximal and distal from the
measurement site. An increase in distal resistance alone would result
in an increase in Plymph. However,
if stretching of the muscle tissue affects both inflow and outflow
resistances similarly, this stretching effect on resistance will not
alter Plymph. The same reasoning
makes it very unlikely that an increased bulging and stretching during
aortic clamping caused the increased sensitivity of
Plymph to
PLV.
In addition, Doucette et al. (2) reported that the wall thickening
waveform during lidocaine administration was similar at low
PLV (average systolic value 49 mmHg) and at normal PLV (87 mmHg). The percent wall thickening during systole did not differ significantly in both situations, i.e., 2.3 ± 3.0 versus 4.0 ± 3.4% (2). Moreover, as noted in
Experimental limitations, wall
thickness did not change in midsystole, while
Plymph followed more or less the
PLV waveform. It
seems therefore that the noncontracting region of the left ventricle is
already maximally stretched at normal
PLV and is not further stretched
during clamping.
During control conditions, the average ratio of pulse
Plymph to pulse
PLV was 0.063 ± 0.03. This
value is similar to a ratio of 0.069 ± 0.013 reported by Han et al.
(3). When regional contraction was impaired with lidocaine, the ratio
of pulse Plymph to
PLV increased to 0.15 ± 0.09. This twofold increase is lower than the 10-fold increase in
Plymph relative to
PLV (i.e., 0.76 ± 0.16) that
was found during induced long diastoles (3). This indicates that there
still was substantial shielding of left ventricular pressure after the
administration of lidocaine. This shielding may be caused by the
stretching of the noncontracting tissue during systole. As depicted in
Fig. 2, the influence of left ventricular pressure on lymph pressure
was found to relate to the contractile state of the myocardium: when
contractility is diminished, the sensitivity of lymph pressure for left
ventricular pressure is enlarged. This finding supports the hypothesis
that, during normal, unimpaired cardiac contraction, stiffening of the
ventricular wall during systole provides a rigid shield for
intramyocardial vessels against deformation by transmission of left
ventricular pressures and other forces (2, 6, 11).
Cardiac contraction and interstitial volume.
The importance of cardiac contraction in stabilizing myocardial
interstitial volume is exemplified by the observation that the water
content increases when the heart is arrested for a period of minutes to
hours (9, 10, 12, 14). The increase in interstitial volume during
cardioplegic arrest can partly be explained by a decrease in myocardial
lymph flow (9, 10). It is suggested by Mehlhorn et al. (9) that,
besides impairment of lymph drainage, the increase in interstitial
volume results from an increased microvascular fluid filtration rate
because of an increase in the duration of diastole and hence the time
for filtration. In contrast to cardioplegic studies (9, 10) in which
animals are placed on cardiopulmonary bypass, resulting in arrest of
the whole heart and abolition of left ventricular pressure development, lidocaine administration in the LAD results in impairment of
contraction of only a part of the left ventricle. Left ventricular
pressure, albeit somewhat reduced, is still generated by the unaffected part of the left ventricle. After lidocaine, heart rate increased and
the diastolic time fraction decreased as shown in Table 1. As a result,
it is not very likely that the increase in
Plymph after lidocaine is caused
by an increased microvascular fluid filtration caused by a change in
diastolic time. One may argue that locally reduced contractility
resembles diastole for that part of the wall. However, it should be
noted that Plymph stabilized ~20
s after the administration of lidocaine (Fig. 1). This observation is
in contrast to the finding that the myocardial interstitial volume
increases steadily during cardioplegic arrest over longer periods of
time.
Because of the low rate of myocardial lymph flow, several investigators
have estimated changes in lymph flow by timed volume collection over
seconds to minutes (7, 9, 10). In this way, continuous information on
the fluid balance of the heart is not obtained. In contrast, lymph
pressure measurements can be used to derive instantaneous information
on factors involved in the myocardial interstitial fluid balance. In a
previous study, it was demonstrated that increases in microvascular
fluid filtration, induced by histamine infusion, coronary venous
pressure elevation, and reactive hyperemia, resulted in fast increases
in lymph pressure (13). It is therefore not unlikely that an increase
in lymph pressure in the present study also reflects an increase in
interstitial pressure. An increase in interstitial pressure is expected
to diminish the transcapillary hydrostatic pressure difference and to
enhance the drainage of lymph fluid, thereby constituting an important
safety factor against the formation of myocardial edema (1, 7).
However, the observed increase in lymph pressure after lidocaine does
not necessarily result in an increase in lymph flow. As suggested in
Interpretation of experimental
findings, systolic bulging of the noncontracting tissue
after the lidocaine might have deformed the myocardial lymphatics,
thereby increasing their resistance, and impairing lymph outflow.
In conclusion, the sensitivity of lymph pressure for left ventricular
pressure is increased during local impairment of cardiac contraction
after administration of lidocaine. The results suggest that the
transmission of left ventricular pressure to the myocardial lymphatics
depends on the contractile state of the myocardium. It seems therefore
that during normal, unimpaired contraction, lymph vessels are shielded
from high systolic left ventricular pressure by the myocardium itself.
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ACKNOWLEDGEMENTS |
The authors thank Aart Boekee for technical assistance during the
experiments and Hans Vink for critical review of the manuscript.
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FOOTNOTES |
Address for reprint requests: J. A. E. Spaan, Dept. of Medical
Physics, Univ. of Amsterdam, Academic Medical Center, PO Box 22700, 1100 DE Amsterdam, The Netherlands (E-mail: J.A.Spaan{at}amc.uva.nl).
Received 27 January 1997; accepted in final form 5 September 1997.
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Effects of crystalloid, blood, and University of Wisconsin perfusates on weight, water content, and left ventricular compliance in an edema-prone, isolated porcine heart model.
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AJP Heart Circ Physiol 274(1):H187-H192
0363-6135/98 $5.00
Copyright © 1998 the American Physiological Society
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Abstract
Introduction
