Download Mechanical Interactions between Four Heart Chambers with and

86
Mechanical Interactions between Four Heart
Chambers with and without the Pericardium
in Canine Hearts
YUKIO MARUYAMA, KOUICHI ASHIKAWA, SHOGEN ISOYAMA, HIROSHI KANATSUKA,
EIJI INO-OKA, AND TAMOTSU TAKISHIMA
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SUMMARY By using excised postmortem hearts obtained from 15 mongrel dogs with the pericardium
intact, we investigated mechanical interactions between the four heart chambers from the standpoint
of ventricular pressure-volume relationships. The interactions investigated were those between (1) the
atrium and the ventricle, (2) the right ventricle and left ventricles, (3) the atrium and one ventricle vs.
the other ventricle, and finally (4) the left and right atrium and the right ventricle vs. the left ventricle.
For these purposes, we inserted compliant balloons into the four heart chambers without injuring the
pericardium, i.e., we incised the base of the atria which was not covered with the pericardium. We
obtained the right and/or left ventricular pressure-volume relationships under a constant pressure in
three other heart chambers by changing the height of the reservoir connected to each balloon. As a
result, both ventricular pressure-volume relationships were hardly affected by an increase in the atrial
pressure ranging from 5 to 30 cm H2O with the pericardium removed, although the ventricle became
less compliant due to an increase of the same magnitude of the opposite ventricular pressure. On the
other hand, the effect of an increase in atrial pressure was distinct with the pericardium intact. Also,
all mechanical interactions were enhanced dramatically with the intact pericardium. Thus, the pericardium plays an important role in these mechanical interactions, especially when the filling pressures
of all heart chambers increase simultaneously. Clinically, these findings may be important to understanding ventricular functions as related to various heart disease—especially acute heart failure.
Circ Res 50: 86-100, 1982
ALTHOUGH the mechanical interaction of heart
chambers in diastole has been demonstrated clinically (Bernheim, 1910; Rao et al., 1968, Herbert et
al., 1969; Olivari et al., 1978) and experimentally
(Moulopoulos et al., 1965; Laks et al., 1967; Taylor
et al., 1967; Bemis et al., 1974; Elzinga et al., 1974),
most studies reported in the literature have focused
on the mechanical interaction between the right
ventricle (RV) and left ventricle (LV).
The mechanism of mechanical interaction has
been considered to be due mainly to anatomic continuity of the heart muscle (Taylor et al., 1967; Laks
et al., 1967). Since the heart is comprised of four
heart chambers (i.e., the right atrium (RA), the left
atrium (LA), the RV, and the LV), it is reasonable
to assume that there are other interactions of heart
chambers in addition to ventricular interplay. Clinically, an increase in filling pressures of all four
heart chambers is very common in heart failure. A
loading of one chamber alone may occur in the
early phases of various heart diseases: for example,
the LA, the RA, the RV, and the LV in mitral,
From the First Department of Internal Medicine, Tohoku University
School of Medicine, Sendai, Japan.
Address for reprints: Tamotsu Takishima, M.D., First Department of
Internal Medicine, Tohoku University School of Medicine, 1-1 Seiryomachi, Sendai 980, Japan.
Received September 23, 1980; accepted for publication September 17,
1981.
tricuspid, pulmonary, and aortic valvular diseases,
respectively.
However, it is not clear either qualitatively or
quantitatively how ventricular pressure-volume (PV) relationships of the LV and RV change in various
pathological situations. A definite change of ventricular compliance may occur, especially after a
simultaneous increase of the filling pressure of two
or three heart chambers. In addition, the heart is
covered with the pericardium. Although the restraining effect of the pericardium has been pointed
out (Holt, 1970; Glantz et al., 1978; Mirsky and
Rankin, 1979; Ross, 1979; Janicki and Weber,
1980a), the importance of the role of the pericardium in such various interactions of heart chambers
is still unknown (Ross, 1979).
Thus, the purpose of the present study is to
define the mechanical interactions of the four heart
chambers and the role of the pericardium in those
mechanical interactions. For this purpose we used
excised postmortem hearts not affected by rigor
mortis, and avoided humoral, neural, pulmonary,
and systemic circulatory effects. Furthermore, we
did not want to injure the pericardium because
preliminary experiments showed that only by opening the pericardium, and thereafter suturing the
pericardial incisions, did the ventricles become less
compliant. Therefore, we tried to keep it completely
intact. As a result, we were able to show the role of
MECHANICAL INTERACTIONS BETWEEN FOUR HEART CHAMBERS/Marayama et al.
the pressure rise of the atrium, the opposite ventricle, and the simultaneous increase in pressure in
those chambers for the RV or LV P-V relationships,
and we definitely demonstrated that the pericardium played an important role in those mechanical
interactions.
Methods
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Experimental Procedure
The isolated heart preparation that we used is
shown schematically in Figure 1. Fifteen mongrel
dogs of both sexes, weighing between 12 and 21 kg
(mean ± SEM: 15.1 ± 0.5 kg), were anesthetized with
pentobarbital sodium (30 mg/kg, iv). The trachea
was intubated and ventilation was maintained with
a Harvard respiratory pump. After a bilateral thoracotomy, heparin (5000 U) was injected, and then
the heart was excised with the lung. We were careful
that the pericardium remained intact during this
procedure.
The excised heart was quickly immersed in a cold
saline bath of about 4°C, and this temperature
remained almost constant throughout the experimental preparation. Then we excised the lung and
searched for the pericardium free areas at the LA
and the RA, which were not covered by the pericardium. We carefully made small incisions in these
areas of each atrium (less than 10 mm in length)
without damaging the pericardium [Fig. 2(1)].
Through these slits in both atria, we intended to
insert thin rubber plugs. Prior to this procedure,
the chordal attachments of the respective papillary
muscles were severed [Fig. 2(2)], and we sutured
thin rubber plugs (2 cm in diameter and 1.5 mm
thick) to the mitral and tricuspid valvular rings
[Fig. 2(4,5)]. By this procedure, the heart was diI
RV P-V RELATION
II LV
vided into four chambers (i.e., the LA, RA, LV, and
RV) without distorting the anatomy. Then we inserted a compliant balloon (0.03 mm thick) into
each chamber. That is to say, we inserted balloons
into the atria through the atrial slits and into the
ventricles through the aortic or pulmonary arterial
roots [Fig. 2(6,7)]. To prevent the balloons from
bulging from the chambers, we securely tied all
vessels connected to the heart except for the aorta
and pulmonary artery.
Experimental Set-up
The tubes connected with the balloons in the
atrial chambers were pulled out from the incised
areas of both atria and connected to each reservoir.
After that, those incised portions were sutured
loosely, and we took care to see that the balloons
were not bulging out from the atria. The connecting
tubes for the balloons in the RV and LV were pulled
out through the ascending aorta and the main pulmonary artery, respectively, and connected to the
reservoir and the system to measure the P-V relationship. We were able to set the height of each
reservoir at will. Then, we ligated both the aorta
and pulmonary artery beyond the orifice of those
valves, and finally transferred the heart into the
other saline bath. The temperature of the saline
was kept at about 17°C throughout the experiment.
The base of the heart was positioned at the surface
level of the saline.
After measuring the ventricular P-V relationships, we inserted two cannulas (Teflon tubes: i.d.
0.9 mm, o.d. 1.2 mm) for the measurement of the PV relationship of the pericardium. In preparation
for this, we made two needle punctures beforehand
(15 mm or more apart). After inserting the cannulas,
P-V RELATION
LVV
RVV
RA: RIGHT ATRUM
RV-RIGHT VENTRICLE
87
LVV
LA:LEFT ATRUM
LV:LEFT VENTRICLE
FIGURE 1 Schematic drawing of the experiment. The RV (I) and LV (II) P-V
relationships were investigated with the
pericardium intact in excised canine
hearts by changing the height of reservoirs of each heart chamber. After that,
P- V relationships for both ventricles were
also investigated without the pericardium.
CIRCULATION RESEARCH
88
VOL.50, NO. 1, JANUARY
1982
0)
FIGURE 2 The figure shows schematically how the thin rubber plug is attached
to the valvular ring, and also how the
compliant balloons are inserted into the
atrium and the ventricle without injuring
the pericardium. As described in Methods, the balloons into the R V and the L V
were inserted from the aorta and pulmonary artery (which are not shown in the
figure), respectively. A, atrial slit; B, compliant balloon; R, thin rubber plug; P,
pericardium; T, tendinous portion; V, tricuspid or mitral valve. See text for details.
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we tied them securely onto the pericardium with a
thin thread. Due to this procedure, compliance of
the pericardium might have been changed slightly.
At the same time, however, we prevented saline
from leaking from the pericardial space. One cannula was connected to a pressure transducer and
the other to the infusion pump. Eleven hearts thus
were successfully prepared.
Pressure-Volume Relationships
Ventricular pressures were measured with a
strain gauge pressure transducer (Toyo Sokki MPU
0.5) and ventricular volumes were measured by a
syringe system which was attached to an infusion
pump (Erma Optical Works Ltd., type SU-105).
After replacing the heart in the bath, we repeated
the infusion and withdrawal of the saline from the
balloon in the ventricular chamber, while the pressures of other chambers were held constant at 5 cm
H2O. Within about 10-15 minute after replacement,
we had stale P-V curves and started measuring the
P-V relationship.
We obtained P-V curves with an infusion pump
at a constant speed of 26.5 ml/min. The pressure
range investigated for the P-V relationships was
about 0-40 cm H2O.
In the pericardial P-V relationship experiments,
the pericardial pressure was measured after the
addition of small amounts of saline. The pericardial
volume was estimated from the total volume: the
volume of four chambers occupied with the saline,
the heart muscle itself, taking the gravitational
effect as 1.0, and the volume of the saline injected
into the pericardial space.
To get an accurate measurement of the P-V
relationship of the pericardium itself, we kept the
volume of the four heart chambers constant by
clamping the connecting tubes at a constant filling
pressure of 5 cm H2O, and therefore the content of
the saline in each heart chamber did not change
during the procedure.
The balloon and associated tubing inserted into
the LA, RA, LV, and RV displaced 3, 4, 8, 9 ml,
respectively, and these increments were added to
all observed volumes. The balloons were quite large
relative to the filling volumes employed so that
there would be no effect on the measurement of
ventricular P-V relationship.
Experimental Protocols
We set the experimental protocol number (Exp.
Prot. No.) from 1 to 20, as demonstrated in Table
1. We investigated RV and LV P-V relationships of
filling pressure ranging from approximately 0 to 40
cm H2O, while we held the filling pressure for other
heart chambers constant at one of three different
values (i.e., 5, 15, and 30 cm H2O) by adjusting the
height of reservoirs. When the filling pressure of all
three heart chambers was set at 5 cm H2O, the
ventricular P-V relationship obtained in that condition was considered to be the control for each
ventricle (i.e., Exp. Prot. No. 1 for the RV; Exp.
Prot. No. 10 for the LV).
Preliminary experiments showed that rigor mortis occurred 2 hours or more after excision of the
heart in this experimental condition, and it proved
impossible to accomplish the whole experimental
procedure from Exp. Prot. No. 1 to Exp. Prot. No.
20 by using the same excised postmortem heart.
Therefore, we divided 15 mongrel dogs into three
experimental groups (five dogs in each group).
Usually, the experimental number of each observation is the same as the number of dogs used in
each experiment. However, because of the mentioned rigor mortis, we observed RV and LV P-V
MECHANICAL INTERACTIONS BETWEEN FOUR HEART CHAMBERS/Maruyama
et al.
89
TABLE 1 Experimental Protocol
Dogs used in each group and experimental
numbers investigated in each protocol
Experimental P-V relations in
1IV or RV
No. indicates pressures
Protocol
no.
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1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
(cm HjO) of each chamber
Group I (n = 5)
Pericard
RA
LA
RV
LV
On
Off
5
15
30
5
5
5
5
5
5
5
5
5
5
15
30
5
15
30
5
15
30
15
30
P-V
P-V
P-V
P-V
P-V
P-V
P-V
P-V
P-V
5
5
5
15
15
15
30
30
30
15
30
5
5
5
15
15
15
30
30
30
P-V
P-V
P-V
P-V
P-V
19
5
5
5
5
5
5
5
5
5
5
15
30
5
15
30
5
5
5
5
5
5
5
5
5
15
30
P-V
P-V
P-V
P-V
P-V
P-V
Group I,[ (n = 5)
Pericard
On
Off
Group III (n = 5)
Pericard
On
Off
6
2
5
4
5
18
5
5
5
5
5
5
5
5
5
4
4
12
5
5
5
5
4
4
4
4
4
RV and LV P-V relations were investigated in Exp. Prot. No. 1-9, and Exp. Prot. No. 10-20, respectively. As for
Exp. Prot. No. 1, for example, 19 and 6 RV P-V measurements keeping the pressure of the RA, LA, and LV at 5 cm
H2O were done in groups I and III (both n — 5) with the pericardium intact, while 5 and 2 RV P-V measurements
at the same pressure of each heart chamber were done with the pericardium removed.
relationships many times at the control state during
each experimental run. As a result, with the intact
pericardium Table 1 shows 19 and 6 RV P-V measurements for Exp. Prot. No. 1 in groups I and III,
respectively, and 18 and 12 LV P-V measurements
for Exp. Prot. No. 10 in groups II and III, respectively. During the time course in groups I and II,
the reduction of ventricular volumes at the highest
pressure (40 cm H2O) attained in the final P-V
relationship was found to be less than 2% of that of
the first experiment. In group III, however, there
was little reduction of ventricular volumes in the
RV or the LV, because the time to accomplish the
experimental procedure in either ventricle was
short. Therefore, reproducibility of the ventricular
P-V relationship was assumed to be quite good in
the three experimental groups.
In group I, we investigated RV P-V relationships
at a constant LA pressure (LAP) of 5 cm H2O when
the RA pressure (RAP) and the LV pressure (LVP)
were changed separately or simultaneously from
Exp. Prot. No. 1 to No. 9. On the other hand, in
group II, we investigated LV P-V relationships at a
constant RAP of 5 cm H2O when the LAP and the
RV pressure (RVP) were changed separately or
simultaneously from Exp. Prot. No. 10 to No. 18. In
group III, we investigated LV and RV P-V relationships at a constant atrial pressure of 5 cm H2O
when only the opposite ventricular pressure increased. In Exp. Prot. No. 19 and No. 20, we investigated LV P-V relationships when filling pressures
of the other three chambers increased simultaneously from 5 to 15 and 30 cm H2O.
Before removing the pericardium, we measured
the P-V relationships of the pericardium in 11 dogs.
After pericardiectomy, we repeated the measurements of ventricular P-V relationships under the
same conditions that had existed with the pericardium intact (Table 1). Finally, we measured heart
weight (HW) in all the experiments (Table 2).
Analysis of Ventricular P-V Relationship
From ventricular P-V relationships, the ventricular volume was measured at every 5 cm H2O of
the ventricular pressure, and all data were expressed as mean ± SEM. Although there was hysteresis between inflation and deflation of the P-V
curves (i.e., ventricular volumes at deflation were
bigger than those at inflation in any given ventricular pressure), we measured ventricular volumes at
only inflation in the present study.
We calculated percent reduction of ventricular
volume after an increase in the atrial and/or the
opposite ventricular pressure as (Vi-V2)/V0 X 100.
Vi equals ventricular volume at a given ventricular
pressure when the opposite ventricular and atrial
pressures are 5 cm H2O, i.e., control state; V2 equals
ventricular volume at the same pressure at which
Vi is obtained, after an increase of the atrial and/or
the opposite ventricular pressure; Vo equals ventricular volume at 5 cm H2O of ventricular pressure at
control state. Percent reduction of each ventricular
CIRCULATION RESEARCH
90
TABLE
2 Heart Weight in Each Experimental Group
Heart wt
(g)
LV+RV+
RA+LA
Group II
(n = 5)
Group I
138.0 ± 16.3
114.0 ± 7.5
A)
LA RA LV (cmHjO)
2:
-40-
119.8 ± 6.1
82.8 ± 10.6
67.2
4.7
71.6 ± 2.9
RV free
wall
31.6 ±4.8
25.6 ± 2.8
25.4 ± 1.7
1982
Right Ventricular Pressure - Volume Relationship
Group III
LV
VOL. 50, No. 1, JANUARY
5
3 : 5
30
5
5 1
Pericard
30
20-
LV weight was measured as the sum of LV free wall and septum.
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volume after an increase of the atrial and/or the
opposite ventricular pressure was calculated with
the pericardium on and off.
To determine whether or not the ventricular PV curves measured during control and other various
interventions were different from each other, we
fitted mean ventricular volumes obtained at each
ventricular pressure of 5-40 cm H2O in Exp. Prot.
No. 1-20 to the following equation derived by
Glantz (1980), i.e.:
p(V) =
3
2
a3V + a2V + a,V + a0) + bS
where s = 1 for the data taken with the pericardium
intact and s = 0 for the data taken after the pericardium was removed. In addition, we strove to
determine the magnitude of the shift of the entire
ventricular p(V) function following an increase in
the atrial pressure and/or the opposite ventricular
pressure. For these purposes, the multiple regression method was employed. This procedure provides a quantitative estimate of the magnitude of
the shift that accompanies intervention. Thus, we
used the data obtained in either ventricle, although
Glantz (1980) adapted this equation only to the
LVp(V) function. Significance was tested by t-statistics, taking the level of P value as 0.05.
Prior to this analysis, using analysis of variance,
we compared ventricular volume at given pressures
from 5 to 40 cm H2O in group I and group II with
intact pericardium for various interventions. For
this analysis, we took into account two factors, i.e.,
the atrial pressure and the opposite ventricular
pressure. Thus, we used a two-way layout in analysis of variance to determine whether or not the
atrial pressure or the opposite ventricular pressure
has an independent effect on the distensibility of
either ventricular chamber. If so, it would be possible to give different values to the shift of the p(V)
function with the fourth order polynomial following
an increase in the atrial pressure or the opposite
ventricular pressure.
Results
Effect of Right Atrial and/or Left Ventricular
Pressures on Right Ventricular P-V
Relationship
With the Pericardium Intact
The RV P-V relationships observed at a constant
LAP of 5 cm H2O are shown in Figures 3 (A) and 4,
10PIO
50
60
80
70
90
Left Ventricular Pressure - Volume Relationship
-40-
X
E
^30CL
1:
2 :
3:
4:
5 :
6 :
RA
5
5
5
LA
5
30
30
RV (cmHiO)
5
Pericard.
5
30
5
5
5
30
30
5
5
30
5
1
J '"'
/
20-
/
/
16
4
ffil
'''' / /'• i
'
// I
/ // 7
/ /
L/
#7
'''
10-
• 13
n
10
20
30
40
50
60
FIGURE 3 The representative data of RV (A) and LV
(B) P- V curves obtained during the inflation in various
conditions of other heart chambers with and without the
pericardium. P-V curves during the deflation shifted to
the right from those of inflation, showing hysteresis
between two curves. However, we showed only the inflation P-V curves for clarity. In Figures 3 (A) and (B),
ventricular P-V relationships were obtained with the
intact pericardium [pericard (+); 1, 2, and 3] and without the pericardium [pericard (-); 4, 5, and 6]. (A)-I:
RV P-V relationship keeping the LAP, RAP, and LVP
at 5 cm H2O. (A)-2: RV P-V relationship keeping the
LAP, RAP, and L VP at 5, 30, and 5 cm H2O, respectively.
(A)-3: RV PV relationship keeping the LAP, RAP, and
LVP at 5, 5, and 30 cm H2O, respectively. (A)-4, 5, and
6: RV P-V relationships without the pericardium at the
same conditions of Figure 3 (A) 1, 2, and 3, respectively.
(B)-l: LV PV relationship keeping the RAP, LAP, and
RVP at 5 cm H2O. (B)-2: LV P-V relationship keeping
the RAP, LAP, and RVP at 5, 30, and 5 cm H2O,
respectively. (B)-3: LV P-V relationship keeping the
RAP, LAP, and RVP at 5, 30, and 30 cm H2O, respectively. (B)-4, 5, and 6: LV P-V relationships without the
pericardium at the same condition of Fig. 3 (B)-l, 2, and
3, respectively. PRV: right ventricular pressure; PhV: left
ventricular pressure; Vnv: right ventricular volume; VLV:
left ventricular volume; see text for details.
MECHANICAL INTERACTIONS BETWEEN FOUR HEART CHAMBERS/Maruyama et al.
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when the RAP and the LVP increased separately
or simultaneously. All data are summarized in
Table 3-1. An increase of the RAP alone resulted
in a significant decrease of the RV volume (RVV)
in any given RVP from 5 to 25 cm H2O when
compared with the control (Exp. Prot. No. 1) [Figs
3(A-2) and 4(A); Table 4]. Also, an increase in the
LVP alone definitely decreased the RVV at any
level of the RVP tested [Figs. 3(A-3) and 4(B);
Table 4]. This trend was similar in other separate
experiments in group III [Exp. Prot. No. 4 and No.
7ofTable3-(3)].
When the degree of the reduction of the RVV
following an increase in the LVP was compared
with that following an increase in the RAP, the
former was much greater even though the magnitude of pressure increase was the same [Figs. 3(A)
and 4]. Furthermore, the combination of an increase
in the RAP and LVP (Exp. Prot. No. 5, No. 6, No.
8, and No. 9) resulted in a definite reduction in the
RVV [Fig. 4(C)]. The greater the increase in pressure in both heart chambers, the larger the reduction of the RVV [Table 3-(l)]. As demonstrated in
Table 4, however, the specific interaction of two
factors, i.e., the RAP and the LVP, for the volume
change in the RVV was not found throughout the
pressure range tested (Table 4).
From the analysis of the equation described in
Methods, it was demonstrated that the effect of the
LVP on the RV P-V relationship was 4 times larger
than that of the RAP. That is, the value of the shift
in the equation was expressed by the weighted
function of the two factors of the LVP and the
RAP, as demonstrated in Table 5-(l) [i.e., pericard
on, 0.45 (LVP-5) vs. 0.11 (RAP-5)].
With the Pericardium Removed
Removal of the pericardium resulted in a downward shift of RV P-V relationship, and the RVV in
each RVP significantly increased at any range of
the RVP, when pressures of the other three chambers were kept at the same level as they had been
with the pericardium intact [Figs. 3 (A) and 4].
After pericardiectomy, the interactions between
the RA and/or the LV vs. the RV became less
prominent: in particular, an increase in RAP had
little influence on the RV P-V relationship [Figs.
4(A, B, and C); Tables 3-(l) and 3-(3)].
Regarding the shift in the equation of the fourth
order polynomial, it was demonstrated that the
shift in the RV P-V relationship following an increase in the RAP or the LVP with the intact
pericardium was larger than it was without the
pericardium [i.e., pericard on 0.46 (LVP-5), 0.11
(RAP-5); pericard off 0.24 (LVP-5), 0.05 (RAP-5)].
As a result, the effect of the RAP became quite
small following pericardiectomy. On the other hand,
the effect of the LVP was still present, showing the
mechanical interaction of the myocardium itself
even after pericardiectomy (P <sc 0.001) [Table 5(1)].
Effect of Left Atrial and/or Right Ventricular
Pressure on Left Ventricular P-V
Relationship
With the Pericardium Intact
The LV P-V relationships are shown in Figures
3(B) and 5, where the LA pressure (LAP) and the
RVP increased separately or simultaneously, while
the RAP was kept at the constant pressure of 5 cm
H2O. An increase of the LAP alone slightly but
significantly decreased the LVV except when the
LVP was 5 cm H2O [Figs. 3(B-2), and 5(A); Tables
3-(2) and 4]. Also, an increase of the opposite ventricular pressure (RVP) definitely decreased the
LVV [Fig. 5(B); Table 4]. When the degree of
pressure increase in the LAP or the RVP was the
RVV mean.SE'-'
<r
60
80
RVV(ml)
100
30
EFFECT OF RAP AND LVP
50
70
RVV(ml)
90
D) RV P-V RELATIONS IN ( t ; (B) AN3(C:
-.40
-40
£20
PERICARD INTACT
70
RVV(ml)
90
30
50
91
70
RVV(ml)
90
FIGURE 4 RV
P-V relationships
from Exp. Group I with and without
the pericardium, when the RAP (A),
the LVP (B), and the RAP and the
LVP (C) were increased, respectively
(n = 5). The figure shows that RV P-V
relationships shift to the left after an
increase of the atrial and/or the opposite ventricular pressure. If the increment of the pressure is the same,
the effect of the opposite ventricular
pressure is definitely larger than that
of the atrial pressure (D). When the
pericardium was removed, those mechanical interactions became less
prominent. RW: Right ventricular
volume Per(+): with the intact pericardium RVP: Right ventricular pressure
Per(-): with the pericardium removed
P(HA. LA. LV): Right atrial, left atrial,
and left ventricular pressure.
TABLE 3 Pressure- Volume Relations
(1) Right ventricular volumes (ml) corresponding to each right ventricular pressure
[RVP (cm H2O)]
r rOtOCO!
5
no.
10
15
20
25
35
30
40
Group I ('pericard on)
1
2
3
4
5
6
7
8
9
49.5
48.3
46.1
43.1
41.3
39.2
38.5
37.0
35.7
±
+
±
±
±
±
±
+
±
1
3
7
57.9 ± 5.4
57.5 ± 5.3
54.2 + 4.8
5.3
4.9
5.1
5.0
4.5
4.6
4.8
3.9
4.0
62.7
61.1
59.3
56.1
54.2
50.6
49.0
47.0
44.4
± 6.5
+ 6.3
+ 6.6
±6.4
± 6.3
+ 5.7
± 5.7
± 5.3
± 5.2
70.3
69.0
67.1
64.6
62.9
59.9
56.7
55.1
51.7
+
±
±
±
+
±
±
±
±
7.4
7.4
7.6
7.4
7.0
6.8
6.6
6.3
6.0
75.6
74.5
72.9
70.6
69.2
66.9
62.8
61.4
58.2
±
+
+
±
±
+
±
±
±
8.1
8.1
8.3
7.9
7.6
7.5
7.1
7.0
6.6
79.6
78.6
77.2
75.1
74.2
72.6
67.8
66.8
64.0
±
±
±
±
±
±
±
±
±
8.6
8.6
8.7
8.4
8.1
8.2
7.6
7.5
7.2
82.9
82.0
80.7
79.1
78.4
77.1
72.1
71.4
69.1
± 9.0
±9.1
± 9.1
± 8.8
± 8.6
± 8.7
± 8.0
± 8.0
+ 7.7
85.6
84.7
83.7
82.3
81.8
80.7
76.0
75.4
73.6
±
±
+
±
±
±
±
+
±
9.3
9.4
9.5
9.1
9.0
9.1
8.4
8.4
8.2
87.6
86.9
86.2
84.8
84.5
83.4
79.2
78.7
77.1
±
+
±
±
±
+
±
±
±
9.6
9.6
9.8
9.3
9.3
9.4
8.7
8.7
8.5
Group I (pericard off)
66.6 ± 6.7
66.6 ± 6.6
62.5 ± 5.9
72.4 ± 7.6
71.8 ± 7.5
68.4 ± 6.8
76.8 ± 8.3
76.1 ± 8.2
73.0 + 7.5
80.4 ± 8.8
79.7 + 8.7
76.6 ± 8.0
83.5 ± 9.3
82.7 ± 9.1
79.9 ± 8.5
86.0 ± 9.7
85.2 ± 9.5
82.6 + 9.0
88.3 ± 10.1
87.5 + 9.9
85.1 ± 9.4
35
40
(2) Left ventricular volumes (ml) corresponding to each left ventricular pressure
[LVP (cm H2O)]
Downloaded from http://circres.ahajournals.org/ by guest on June 17, 2017
Protocol
no.
5
10
15
25
20
30
Group II (pericard on)
10
11
12
13
14
15
16
17
18
34.9
34.1
33.2
27.8
28.4
27.5
26.5
26.7
26.0
±
±
±
±
±
±
+
±
±
10
12
18
42.1 ± 1.3
43.2 ± 1.6
39.0 ± 2.1
2.1
2.7
2.1
2.5
2.1
1.8
1.9
1.8
1.7
43.8
42.8
41.4
36.4
35.6
33.9
31.1
31.4
30.0
±
±
+
±
±
±
±
±
±
2.2
2.5
2.4
2.0
2.1
2.0
2.0
2.0
1.7
49.9
48.8
47.4
43.9
43.1
40.7
37.2
37.1
34.8
±2.1
± 2.4
± 2.4
± 1.9
± 2.1
± 2.3
± 2.1
± 2.2
± 2.1
54.6
53.4
51.9
49.8
49.3
46.9
42.7
42.5
39.9
±
±
+
±
±
±
+
±
±
2.0
2.2
2.3
1.9
2.1
2.3
2.0
2.2
2.2
58.3
57.2
55.6
54.4
53.9
51.8
47.9
47.4
45.1
+
±
±
±
±
+
±
±
+
2.1
2.2
2.4
1.9
2.0
2.2
2.2
2.2
2.3
61.1
60.1
58.5
58.3
57.8
55.9
52.1
51.7
49.8
±
+
±
±
±
±
±
+
±
2.3
2.3
2.5
2.1
2.1
2.3
2.1
2.2
2.3
63.5
62.4
61.0
61.1
60.7
59.0
55.8
55.4
53.7
± 2.5
± 2.5
+ 2.6
±2.2
± 2.3
± 2.5
± 2.2
± 2.3
± 2.4
65.2
64.4
63.1
63.5
63.1
61.5
58.7
58.5
56.9
±
±
±
+
+
±
±
±
±
2.7
2.7
2.8
2.5
2.6
2.7
2.4
2.4
2.5
Group II (pericard off)
51.0 ± 1.5
51.6 ± 1.6
46.8 ± 2.3
56.7 ± 0.6
56.9 ± 1.8
52.4 ± 2.5
60.7 ± 1.9
60.7 ± 2.1
56.7 + 2.6
63.6 ± 2.2
63.5 ± 2.3
60.1 ± 2.7
65.6 ± 2.3
65.8 ± 2.6
63.1 ± 2.9
67.8 ± 2.7
67.7 ± 2.8
65.3 ± 3.0
69.4 ± 2.9
69.1 ± 3.0
67.3 ± 3.2
(3) Right (Exp. Prot. No. 1, 4, 7) or left (Exp. Prot. No . 10, 13, 16, 19, 20) ventricular volumes (ml) corresponding to
each ventricular pressure [RVP or LVF• (cm H2O)]
no.
5
10
15
20
35
30
25
40
Group III (pericard on)
1
4
7
10
13
16
19
20
44.1
38.8
34.3
31.1
24.3
23.2
24.3
20.0
±
±
±
±
±
±
±
±
3.5
3.2
2.9
1.0
2.6
2.2
2.4
3.1
52.6
47.3
41.4
41.9
35.0
30.5
34.1
25.9
±
±
±
±
±
±
±
±
2.3
2.7
2.3
1.4
2.4
2.8
1.8
2.0
57.6
53.0
46.9
49.2
43.1
37.9
43.9
32.8
±
±
±
±
±
±
±
±
2.3
2.6
2.1
1.9
3.0
3.4
3.0
2.4
61.4
57.7
51.1
54.3
49.2
43.9
50.1
39.5
1
7
10
16
20
43.7
41.7
36.6
32.1
29.2
±
±
±
±
±
2.7
3.9
1.7
2.3
0.7
53.6
51.5
48.3
44.0
41.5
±
±
±
±
±
0.9
1.5
2.4
2.3
2.7
59.4
57.1
54.9
50.9
48.9
±
±
±
±
±
3.3
1.5
3.1
3.0
3.9
63.5
60.9
59.9
56.1
54.4
±
±
+
+
±
±
±
±
2.6
2.7
2.0
2.3
3.5
3.8
3.7
3.2
64.5
61.1
54.7
58.3
54.2
48.7
55.5
45.1
+
±
±
±
±
±
+
±
3.0
2.9
2.0
2.5
3.8
3.9
4.5
3.8
67.0
64.1
57.8
61.4
58.2
53.0
59.4
50.3
± 3.3
±3.1
± 2.1
± 2.7
± 4.2
± 4.1
± 5.0
± 4.4
69.0
66.6
60.6
63.7
61.3
56.9
62.9
54.5
±
±
±
±
±
±
±
±
3.5
3.4
2.4
2.9
4.6
4.3
5.5
4.6
70.8
68.5
63.0
65.7
64.0
60.2
65.2
59.0
±
+
±
±
+
±
±
±
3.8
3.7
2.6
3.1
4.9
4.5
5.8
5.6
69.1
66.5
65.8
63.1
61.9
±
+
±
±
±
71.4
68.8
67.9
65.4
64.6
±
±
±
±
±
7.6
2.7
4.8
4.8
6.3
73.1
71.1
69.6
67.4
66.9
+
±
±
±
+
7.8
2.9
5.0
4.9
6.6
Group III (pericard off)
±
±
±
+
±
4.8
1.7
3.8
3.6
4.8
66.6
64.1
63.3
60.0
58.6
±
±
±
+
±
5.9
2.1
4.2
4.3
5.5
6.8
2.3
4.6
4.7
6.0
(4) Pericardial volumes (ml) corresponding to each pericardial pressure (cm H2O)
Pericardial pressure
10
5
Pericardial
volume
251.8. ± 11.8
266.4 ± 11.7
Data are expressed as mean ± SEM.
15
275.2 ± 12.4
20
25
30
35
40
281.3 ± 12.8
286.0 ± 13.0
290.1 + 13.1
293.8 ± 13.4
296.9 + 13.4
MECHANICAL INTERACTIONS BETWEEN FOUR HEART CHAMBERS/Maruyama
et al.
93
4 Test of Significance in Right or Left Ventricular Volumes (ml) for Each
Ventricular Pressure Following an Increase of Atrial and/or Opposite Ventricular
Pressure
TABLE
Grand mean
± SEM
RVP (cm H,O)
25
20
5
10
15
42.098
2.292
53.84
2.387
61.94
2.481
68.02
2.583
72.90
2.503
30
35
40
77.00
2.414
80.43
2.196
83.16
1.990
Group I (pericard on)
Significance
LVP(-) vs.
LVP(+)
RAP(-) vs.
RAP(+)
Interaction
[LVP(+) X RAP(+)]
**
**
**
**
* t
**
**
**
**
*•
**
*
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
NS
5
10
15
LVP (cm H2O)
25
20
30
35
40
29.48
1.427
36.29
1.336
42.58
1.186
56.17
0.952
59.22
0.877
61.67
0.788
**
**
**
**
**
**
NS
NS
NS
(b) Group II (pericard on)
Downloaded from http://circres.ahajournals.org/ by guest on June 17, 2017
Grand mean
± SEM
47.91
1.129
52.43
1.027
Group II (pericard on)
Significance
RVP(-) vs.
LVP(+)
LAP(-) vs.
LAP(+)
Interaction
[RVP(+) x LAP(+)]
**
**
**
NS
**
• *
**
NS
NS
NS
NS
• *
NS
The effect of an increase of LVP, RAP, RVP, and LAP on RV or LV volumes was compared at each ventricular
pressure with the presence (+) of the pressure load indicated and the control state (—). Data were the same with
Tables 3-(l) and (2) (pericard on). Significance was tested by analysis of variance, as stated in Methods.
• P < 0.05; '• P< 0.01; NS, not significant.
same, the magnitude of its effect on LV P-V relationship was much more prominent after an increase of the RVP than after an increase of the
LAP [Figs. 3(B) and 5; Table 3-(2)].
When the LAP and the RVP increased simultaneously, the resultant LV volume considerably decreased, as found in Exp. Prot. No. 18 [Figs. 3(B)
and 5(C)]. However, the specific interaction of the
LAP and the RVP was not demonstrated (Table 4).
With the pericardium closed, when an increase of
the opposite ventricular pressure was the same, the
percent decrease in LVV after an increase in RVP
was larger than the decrease in RVV after an increase in LVP (Fig. 6).
Values indicating quantitatively the shift in the
LV P-V relationship after an increase in the LAP
or the RVP are shown in Table 5-(l). The effect of
the opposite ventricular pressure was 4 times larger
than that of the atrial pressure [i.e., 0.43 (RVP-5)
vs. 0.11 (LAP-5)]. This trend was almost the same
as found in the RV P-V relationships.
With the Pericardium Removed
Removal of the pericardium resulted in a downward shift of the LV P-V relationship as demon-
strated in the RV P-V relationship after pericardiectomy (Figs. 3(B) and 5). Thus, as shown in
Table 3-(2), the LVV increased tremendously after
pericardiectomy at any given LVP.
Moreover, when the pericardium was removed,
the magnitude of the interactions between the cardiac chambers definitely weakened. Especially, the
effect of atrial pressure on the LV P-V relationship
almost disappeared [Fig. 5(A); Table 3-(2)].
As previously described in cases with the intact
pericardium, the percent reduction in the LVV after
an increase in the RVP was also larger than that of
the RVV following an increase in the LVP, when
an increase in the opposite ventricular pressure
compared is the same [Fig 7(A and D)].
As shown in Table 5-(l), the effect of the atrial
pressure and the opposite ventricular pressure on
the LV P-V relationships decreased after pericardiectomy, i.e., the effect of the LAP was extremely
small [0.007 (LAP-5)], whereas that of the RVP was
about two-thirds [0.28 (RVP-5)], compared with
corresponding values before pericardiectomy [i.e.,
0.44 (RVP-5), 0.14 (LAP-5)]. Thus, even though the
pericardium was removed, there was still a mechanical interaction between both ventricles (P « :
0.001).
CIRCULATION RESEARCH
94
TABLE 5
1982
The Fourth Order Polynomial and the Magnitude of the Shift Following Various Interventions
Pericard on
or off
(Exp. Prot. No.)
Exp.
group
VOL.50, No. 1, JANUARY
LV p(v)
or
RV p(v)
Fourth order polynomial
(1) Effect of the atria] pressure or the opposite ventricular pressure
(a) With the pericardium
I Pericard on
RV p(v) = [-0.OO0OO75RVV4 + 0.002217RVV3
(No. 1-No. 9)
n
r
SE
72
0.9927
1.46
0.45(LVP - 5); P «
0.001
0.1KRAP - 5 ) ; P «
0.001
72
0.9944
1.28
0.43(RVP - 5); P «
0.001
0.11 (LAP - 5 ) ; P «
0.001
88
0.9906
1.65
-0.0087(RAP - 5); NS
0.42(RVP - 5); P «
0.001
0.11 (LAP - 5); P «
0.001
24
0.9914
1.73
0.525(LVP - 5);
P « 0.001
24
0.9925
1.62
0.377(RVP - 5);
P « 0.001
-0.2227RVV2 + 9.90RVV - 166.4]
Significance
+0.45(LVP - 5) + 0.1KRAP - 5)
II
Pericard on
(No. 10-No. 18)
LV p(v) = [ -0.OO0012LVV4 + 0.003000LVV3
2
-0.2418LVV + 8.75LVV - 117.4]
+0.43(RVP - 5) + 0.1KLAP -5)
II + III
Downloaded from http://circres.ahajournals.org/ by guest on June 17, 2017
Pericard on
(No. 10-No. 20)
LV p(v) = [ 0.0000091 LVV" - 0.001207LVV3
+0.0630LVV2 - 0.77LVV - 9.1]
-0.0087(RAP - 5) + 0.42(RVP - 5)
+0.1KLAP - 5)
III
Pericard on
(No. 1,4,7)
Pericard on
(No. 10,13,16)
I
Pericard on
(No. 1,3,7)
Pericard off
(No. 1,3,7)
II
Pericard on
(No. 10,12,18)
Pericard off
(No. 10,12,18)
RV p(v) = [-0.0000236RVV + 0.005694RVV'
-0.4795RVV2 + 17.95RVV - 256.5]
+0.529(LVP - 5)
LV p(v) = [ -0.0OO0O976LVV4 + 0.002270LVV3
-0.168LVV2 + 5.67LVV - 70.0]
+0.377(RVP - 5)
(b) With the pericardium and without the pericardium
RV p(v) = [-0.0000097RVV4 + 0.002866RVV'1
24 0.9918 1.74
-0.2928RVV2 + 13.14RVV - 220.4]
+0.46(LVP - 5) + 0.11 (RAP - 5)
RV p(v) = [-0.000142RVV4 + 0.042253RVV3
Pericard
on/off
(No. 10)
Pericard
on/off
(No. 12)
0.9898
1.94
0.24(LVP- 5 ) ; P «
0.001
0.05(RAP - 5); NS
24
0.9957
1.26
0.44(RVP - 5); P «
0.001
0.14(LAP- 5 ) ; P «
0.001
24
0.9963
1.17
0.28(RVP - 5); P «
0.001
0.007(LAP - 5); NS
16
0.9943
1.55
b = 3.13; P < 0.002
16
0.9924
1.78
b = 5.17; P « 0.001
16
0.9956
1.35
b = 12.40; P « 0.001
16
0.9978 0.97
16
0.9942
-4.6351RVV + 223.62RVV
- 4011.3]
+0.24(LVP - 5) + 0.05 (RAP - 5)
2
-0.3644LVV + 13.11LVV - 175.7]
+0.44(RVP - 5) + 0.14(LAP - 5)
LV p(v) = [ -0.000024LVV4 + 0.007232LVV3
2
-0.7066LVV + 28.95LVV - 428.7]
+0.28(RVP - 5) + 0.007(LAP - 5)
(2) Effect of the pericardiumL
I Pericard
RV p(v) = [0.0000054RVV4 - 0.000791RVV3
on/off
+0.0356RVV2 - 0.024RVV - 20.8]
(No. 1)
+3.13S
Pericard
RV p(v) = [0.0000044RVV4 - 0.000528RVV3
+0.0122RVV2 + 0.906RVV - 36.0]
on/off
(No. 3)
+5.17S
Pericard
RV p(v) = [0.0000117RVV4 - 0.002444RVV3
on/off
+0.0196RVV2 - 6.491RVV + 65.6]
(No. 7)
+ 12.40S
II
24
2
LV p(v) = [ -0.0000186LVV4 + 0.004490LVV3
LV p(v) = [ 0.0000163LVV4 - 0.001738LVV3
+0.0392LVV2 + 1.716LVV - 60.1]
+7.24S
LV p(v) = [ 0.0000202LVV4 - 0.002767LVV3
+0.1341LVV2 - 1.825LW - 16.5]
+ 11.04S
0.46(LVP- 5 ) ; P «
0.001
0.11(RAP- 5 ) ; P «
0.001
1.57
b = 7.24; P « 0.001
b = 11.04; P « 0.001
MECHANICAL INTERACTIONS BETWEEN FOUR HEART CHAMBERS/Maruyama
et al.
95
TABLE 5—continued
Pericard on
or off
(Exp. Prot. No.)
Exp.
group
III
LV p(V)
or
RV P(v)
Fourth order polynomial
Significance
3
Pericard
on/off
(No. 18)
LV p(v) = [ 0.0000116LVV - 0.001120LVV
+0.1545LVV2 + 2.083LVV - 60.9]
+ 15.47S
16
Pericard
on/off
(No. 10)
Pericard
on/off
(No. 16)
Pericard
on/off
(No. 20)
LV p(v) = [ -0.0OO0165LVV + 0.004284LVV3
-0.3650LVV2 + 13.26LVV - 172.2]
+3.76S
LV p(v) = [ -0.0000168LVV + 0.003548LVV3
-0.2547LVV2 + 8.21LVV - 97.4]
+8.54S
LV p(v) = [ -0.0000008LVV + 0.000587LVV3
-0.0575LVV2 + 2.65LVV - 40.5]
+ 12.27S
16 0.9970 1.12
b = 3.76; P « 0.001
16
b = 8.54; P « 0.001
0.9983 0.85
0.9920 1.83
16 0.9942 1.56
Downloaded from http://circres.ahajournals.org/ by guest on June 17, 2017
(3) Effects of the pericardium, the opposite ventricular pressure, and the atrial pressure
I Pericard
RV p(v) = [0.0OOO0033RVV4 + 0.0O0463RVV3
48 0.9791 2.55
on/off
-0.0794RVV2 + 4.78RVV - 104.1]
(No. 1, 3, and 7)
+6.42S + 0.347(LVP - 5)
+0.084(RAP - 5)
II
III
b = 15.47; P« 0.001
b = 12.27; P « 0.001
b = 6.42; P « 0.001,
0.347(LVP - 5);
P « 0.001
0.084(RAP - 5); P <
0.05
Pericard
on/off
(No. 10,12, and
18)
LV p(v) = [ 0.O0O0285LVV - 0.004169LVV3
+0.2152LVV2 - 3.637LVV - 6.8]
+ 10.90S + 0.346(RVP - 5)
+0.073(LAP - 5)
48 0.9875 1.97
b = 10.90; P « 0.001,
0.346(RVP - 5);
P « 0.001
0.073(LAP - 5); P <
0.02
Pericard
on/off
(No. 10,16 and 20)
LV p(v) = [ 0.0000086LVV - 0.000991LVV
+0.0363LVV2 + 0.265LVV - 25.0]
+7.82S + 0.276(RVP - 5)
+0.112(ATRIAL*P - 5)
48 0.9815 2.40
b = 7.82; P « 0.001,
0.276(RVP - 5);
P « 0.001
0.112(ATRIALP - 5);
P « 0.005
The equations of the ventricular p(v) function were expressed by the fourth order polynomial in two cases, i.e., an increase of the atrial pressure and
the opposite ventricular pressure. In addition, the equations were demonstrated with and without the pericardium (1). The effect of the pericardium on the
shift of p(v) function was indicated in (2). In (3), the effects of the pericardium, the atrial pressure, and the opposite ventricular pressure were also shown.
The magnitude of the shift on the entire p(v) function induced by those factors was represented by bS and/or the term of the atrial or ventricular pressure
(cm H2O). ATRIAL'P; In Exp. Prot. No. 20, both the LAP and RAP were increased simultaneously from 5 cm H20 to 30 cm H2O. Thus, we cannot
discriminate one from the other. Therefore, we expressed its effect as "atrial P." RVV: Right ventricular volume (ml), LVV; Left ventricular volume (ml),
RVP; Right ventricular pressure (cm H2O), LVP; left ventricular pressure (cm H2O), RAP; Right atrial pressure (cm H<0), LAP; Left atrial pressure (cm
H2O), S; S = 1 for the data with the pericardium intact and S = 0 for the data without the pericardium.
Concomitant Effect of Left and Right Atrial
and Right Ventricular Pressures on LV P-V
Relationship
With the Pericardium Intact
In group III, only ventricular interactions were
investigated in the same canine group. As presented
in Table 3-(3), the effect of the opposite ventricular
pressure on both ventricular P-V relationships was
also demonstrated from this experimental run, and
the magnitude of the changes in the ventricular
volume following an increase in the opposite ventricular pressure was almost the same as found in
groups I and II with the intact pericardium.
When the RAP, the LAP, and the RVP simultaneously increased from 5 cm H2O to 15 and 30 cm
H2O (Exp. Prot. No. 19 and No. 20), the LVV
resulted in a definite reduction at any level of the
LVP values from 5 to 40 cm H2O [Table 3-(3); Fig.
The effects of the RAP, LAP, and RVP on the
shift in the LV p(v) function were calculated by
using the data from Exp. Prot. No. 10 to Exp. Prot.
No. 20 in groups II and III. It was demonstrated
that the effect of the RAP on the LV P-V relationships was significantly smaller than that of the RVP
or the LAP, and no significant effect of the RAP on
the shift of the LV P-V curves was found [i.e.,
-0.0087 (RAP-5), 0.42 (RVP-5), 0.11 (LAP-5)]
[Table 5-(l)].
With the Pericardium Removed
After the removal of the pericardium, mechanical
interactions also weakened as previously described
[Table 3-(3)]. However, there was still a considerable difference in the LVV between Exp. Prot. No.
10. and No. 20 in any given LVP, showing a distinct
reduction of the LV compliance even without the
pericardium.
P-V Relationship of the Pericardium
The changes in the volumes in the pericardial sac
were demonstrated at every 5 cm H2O of pericardial
CIRCULATION RESEARCH
96
A)EFFECT OF LAP
LVY.meantSEM
B) EFFECT OF RVP
—•
5 5
5 30
cmH20
20
60
LW(ml)
40
80
D) EFFECT OF L A P RAP AND RV=
r
(LARAFW)
o 5 5 5
• 30 30 30
cmH20
f
Downloaded from http://circres.ahajournals.org/ by guest on June 17, 2017
/ * >
o1--
40
60
LVV(ml)
80
10
50
LVV(ml)
30
pressure [Table 3-(4)]. The heart weight was 122.2
± 6.8 g (mean ± SEM).
We found a significant shift in the bS term with
and without the pericardium, as shown in Table 5(2). Following an increase in the atrial pressure
and/or the opposite ventricular pressure, the bS
term became larger in both LV and RV p(v) equations.
.
R V
t
•
-50
First, in our experimental preparations, coronary
perfusion was not maintained. As for coronary perfusion pressure, it has been thought to affect ventricular diastolic compliance (Salisbury et al., 1960;
Morgenstern et al., 1973), although it is still contro-
1
z-40
LA =30
30
O
3-30
!-30
LA.RA=5 LV=30
]\
CC
! • • •
-20
.1
-20
=5
(n=10)
,LA/)A=5RV=15
LA.RA=5 LV=15
-10
-10
[
%
I
T-T-TLA=5RA=30LV=5/
10
20
30
40
R V PRESSUR£(cmH20)
FIGURE 5 LV P-V relationships obtained from Exp. Group II and Group
HI with and without the pericardium,
when the LAP (A), the RVP (B), the
LAP and the RVP (C), and the LAP,
the RAP, and the RVP (D), respectively, increased. Data from (A) to (C)
were obtained from Exp. Group II (n
= 5), while data in (D) were obtained
from Exp. Group III (n = 4). The figure
shows that LV P-V relationships shift
to the left after an increase of the atrial
and/or the opposite ventricular pressure, as demonstrated in RV P-V relationships of Figure 4. When pressure
of two or three heart chambers increased simultaneously f(C) and (D)J,
distensibility of the LV decreased dramatically. Furthermore, it should be
noted that the role of the pericardium
for those mechanical interactions is
quite important.
Limitations of Methods
-50r
Z-40F
70
1982
Discussion
L V
-58.1
— Per!-)
- Per(-)
VOL. 50, No. 1, JANUARY
10
20
30
U0
LV PRESSURE (cmH 2 0)
FIGURE 6 The figure shows that percent reduction of both ventricular volumes with the
intact pericardium after an increase ofpressure
of the heart chamber(s), and percent reduction
of both ventricular volumes from the control
state (i.e., pressure of each heart chamber is 5
cm H2O) was shown at every 5 cm H2O of
ventricular pressure from 5 to 40 cm H2O, when
the atrial and/or the opposite ventricular pressure increased to 15, and 30 cm H2O. The effect
of the opposite ventricle on ventricular P-V
relationships was definitely greater than that
of the atrium. Furthermore, simultaneous increase ofpressure in three heart chambers (i.e.,
the RA, LA, and RV) decreased the LV volume
dramatically (right panel) at any pressure of
the L V from 5 to 40 cm H2O. Numbers used in
the figure indicate pressure (cm H2O) of each
heart chamber (i.e., for example, LA, RA = 5,
LV = 30 means that left and right atrial pressures equal 5 cm H2O, and left ventricular
pressure equals 30 cm H2O), while numbers in
parenthesis indicate experimental numbers
used for the experiments. Data are expressed as
mean ± SEM.
MECHANICAL INTERACTIONS BETWEEN FOUR HEART CHAMBERS/Maruyama et al.
(B)
(A)
-20
(D)
(C)
RAP=3OcmH2O _20
LAP=30
RVP=30
(n=4)
LAP=30
RVP=30
(n=4)
LAP=5
RVP=30
(n=4)
LAP=5
LVP=30
(n=5)
-15
'-15
O
t
tr
I
Downloaded from http://circres.ahajournals.org/ by guest on June 17, 2017
0
102030400
LV
102030
40 0
10203040
PRESSURE ( c m H 2 0 )
97
FIGURE 7 The figure shows that percent
reduction of both ventricular volumes
without the pericardium (removed) after
an increase of pressure of the opposite
ventricle and/or the atrium. The trend
was almost the same as demonstrated in
Figure 6 with the pericardium, although
the magnitude of mechanical interaction
between heart chambers decreased prominently. Data are represented as mean ±
SEM.
0 10 20 30 40
RV PRESSUREUmHjO)
versial (Abel and Reis, 1970; Glantz and Parmley,
1978). From our present results, it is unclear
whether coronary perfusion plays an important role
in the mechanical interaction of the four heart
chambers. In addition, although developed pressure
itself may change ventricular diastolic compliance
(Janicki and Weber, 1977), it also remains to be
clarified how the present results were affected by
ventricular developed pressure. Second, rigor mortis should be taken into account, when excised
postmortem hearts are used. In our preparations, it
was negligible at about 17°C in the water bath until
about 2 hours after the excision of the heart. These
results are in line with previous reports (Griggs et
al., 1960; Laks et al., 1967). Therefore, we considered
its effect to be unimportant for our present experiments. Third, we sutured thin rubber plugs to divide
the heart into four chambers without distortion of
the heart, since distortion of the heart has been
reported to change ventricular compliance (Powell
et al., 1970). However, it is unclear whether our
present method induces other technical errors.
Fourth, our purpose is to clarify the elastic properties of the right and left ventricles following various
interventions. Even though the infusion rate for the
balloons in both ventricles was slow in indicating
ventricular P-V relationships, it seemed to be sufficient for its purpose. Similarly, previous papers
(Taylor et al., 1967; Powell et al., 1970; Spotnitz and
Kaiser, 1971; Santamore et al., 1976; Palacios et al.,
1976; Janicki and Weber, 1980) have also reported
the use of isometric preparations or very slow filling
rates for ventricles tested, because many investigators have concentrated on ventricular diastolic P-V
relations in mid-diastole and late diastole. On the
other hand, it has been shown that not only elastic
but also, viscous, properties play an important role
in ventricular diastolic behavior, especially at the
early or rapid filling phase of ventricular diastole
(Noble et al., 1969; Kennish et al., 1975; Gaasch et
al., 1972; Rankin et al., 1977; Pouleur et al., 1979).
Thus, it is very interesting to speculate how the
present data may be influenced by the participation
of myocardial viscous and/or inertial properties.
Our experimental system, however, is not suitable
for detecting the participation of such properties,
and therefore it remains to be resolved. Fifth, the
present experiments were performed at about 17°C
in order to prevent rigor mortis. This temperature
might change diastolic elastic properties of the myocardium (Templeton et al., 1974), although this
speculation requires further validation in the arrested heart.
Influence of Atrial Pressure on Ventricular
P-V Relationship without the Pericardium
Hitherto, although ventricular interaction has
been demonstrated in experimental studies (Moulopoulos et al., 1965; Taylor et al., 1967; Laks et al.,
1967; Bemis et al., 1974; Elzinga et al, 1974) or
disease states (Bernhein 1910; Rao et al, 1968;
Herbert and Yellin, 1969; Olivari et al, 1978) mechanical interaction of the atrial chamber vs. ventricular chamber has not been investigated thoroughly.
The present study showed that RV and LV P-V
relationships were unaffected by an increase in right
or left atrial pressure alone, if the pericardium was
removed as demonstrated in Tables 3-(l) (2), and 5.
The relative contribution of the pericardium to this
is discussed below.
Influence of the Opposite Ventricular
Pressure on Ventricular P-V Relationship
without the Pericardium
Moulopoulos et al. (1965) showed that left ventricular diastolic pressure began to rise when the
right ventricular diastolic pressure rose to 10 mm
98
CIRCULATION RESEARCH
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Hg, and that it increased even further when right
ventricular diastolic pressure exceeded 10 mm Hg.
Taylor et al. (1967) also reported that the effect of
right ventricular filling on left ventricular diastolic
compliance was not discernible when left ventricular diastolic pressure was low (3 mm Hg) but that,
at a left ventricular diastolic pressure of 20 mm Hg,
left ventricular volume was 7.1% less with the RV
full than with the RV empty. Moreover, Laks et al.
(1967) reported that with infusions into only one
ventricle, right and left ventricular volumes were 20
to 74% greater at 10 mm Hg than when both ventricles were filled simultaneously. Thus, based on
these experimental studies, distensibility of the left
or right ventricle decreased after an increase in the
filling of the opposite ventricle.
Such an effect has been thought to be due to an
influence of right or left ventricular filling on circumferential fibers shared by both ventricles and to
the stiffening of the septum (Taylor et al., 1967;
Laks et al., 1967). Moreover, Santamore et al. (1967)
reported on the displacement of the septum following an increase of the opposite ventricular pressure
in perfused rabbit hearts. Also, Bemis et al. (1974)
demonstrated with the pericardium loosely sutured
that increased right ventricular filling pressure was
associated with a reduction in the septum to free
wall hemiaxis and a corresponding increase in the
anterior-posterior axis of the LV, and as a result
this shape change of the LV was accompanied by a
substantial increase in left ventricular filling pressure. Thus, such factors (i.e., increased septal stiffness or stretching of common fibers, septal displacement) are thought to play an important role in the
mechanical ventricular interaction even without a
clear role of the pericardium.
On the other hand, the magnitude of the influence of the atrial pressure for ventricular P-V relationships was clearly different from that observed
by increasing the opposite ventricular filling pressure [Tables 3-(l) (2) (3), and 5]. Namely, the effect
of the atrial pressure without the pericardium was
quite small and not significant on the shift in the
entire p(v) function. We considered that the difference was due in part to the close anatomical association of both ventricles.
The present results demonstrate that increasing
the LVP decreases RV compliance and also that
varying the RVP changes LV compliance in a reciprocal manner. As for the magnitude of ventricular
interaction, we clearly showed with and without the
pericardium that the percent reduction in the LVV
was much greater than the percent reduction in the
RVV, when an increase of the opposite ventricular
pressure was the same magnitude (Figs. 6 and 7).
Weighted functions of the RVP and the LVP on the
shift of the fourth order polynomial were almost
the same, or the former was smaller than the latter,
as demonstrated in Table 5-(l) [i.e., pericard on:
0.46 (LVP-5) in group I vs. 0.44 (RVP-5) in group
VOL. 50, No. 1, JANUARY 1982
II, 0.525 (LVP-5) vs. 0.377 (RVP-5) in group III;
pericard off: 0.24 (LVP-5) in group I vs. 0.28 (RVP5) in group II]. In addition, we calculated the magnitude of the shift following an increase in LVP on
RV p(v) function by using Exp. Prot. No. 1, 4, 7 in
group I, and also the magnitude of the shift following an increase in RVP on LV p(v) function by
using Exp. Prot. No. 10, 13, 16 in group II. The
magnitudes of the shift were 0.46 (LVP-5) and 0.45
(RVP-5), respectively. Thus, we considered the difference in VO(LV) and VO<RV) (i.e., each ventricular
volume at 5 cm H2O of ventricular pressure at the
control state) to be, possibly, an important factor in
the different responses following an increase in the
opposite ventricular pressure. Our findings are similar to those of Janicki and Weber (1980b), in which
they compared the increase in EDP in the ventricle
with fixed EDV to elevations in EDV in the other
ventricle. The role of the pericardium in this phenomenon is also discussed below.
Function of Pericardium for Mechanical
Interaction
One of the functions that various investigators
have attributed to the pericardium is the prevention
of dilation of the heart chamber, and it has been
thought to have a restraining influence on intrapericardial structures (Holt, 1970; Spotnitz and Kaiser,
1971; Alderman and Glantz, 1976; Glantz et al., 1978;
Mirsky and Rankin, 1979; Ross, 1979; Shabetei et
al., 1979; Janicki and Weber, 1980a). From the
present study, it was clear that the slope of the
pericardial P-V curve became steeper with an increase in infused saline in the pericardial sac [Table
3-(4)]. Those results are in agreement with a previous report (Holt, 1970).
Although the effect of the atrial pressure on the
opposite ventricular P-V relationship was shown by
Elzinga et al. (1974), its mechanism was thought to
be induced through a change in the ventricular enddiastolic P-V relationship of the opposite ventricle.
Thus, direct interaction of the atrium and the ventricle has not been elucidated.
As demonstrated in Table 5, the effect of the
LAP on the shift in the LV P-V relationships without the pericardium was quite small, compared with
that obtained with the pericardium intact. Also, the
effect of the RAP with the pericardium intact was
almost 2 times larger than that without the pericardium. As a result, the significance of the effect of
the atrial pressure on the shift in the entire p(v)
function was not found. Thus, we considered the
direct mechanical interplay of the atrium and the
ventricle to be due mainly to the restraining effect
of the pericardium.
As for the ventricular interaction, it has been
thought that such interaction is present even with
the pericardium removed. However, if the pericardium is not present, it has been thought that the
opposite ventricular filling pressure affects the left
MECHANICAL INTERACTIONS BETWEEN FOUR HEART CHAMBERS/Maruyama et al.
Downloaded from http://circres.ahajournals.org/ by guest on June 17, 2017
or right ventricular distensibility only at a high
range of left ventricular diastolic pressure (Moulopoulos et al, 1965; Taylor et al, 1967; Laks et al,
1967; Santamore et al, 1976). In contrast to previous data, ventricular interaction was found at any
filling pressure, when the opposite ventricular pressure increased to 15 cm H2O or more [Table 5],
even if the pericardium was removed. This interaction was also enhanced with the pericardium
intact. Specifically, although a significant restraint
by sutured pericardium has been demonstrated
(Stokland et al, 1980), it should be noted that the
quantitative effects of the presence of the pericardium for those various interactions were obtained
in the present study without incision, because the
pericardium was not opened, and therefore the pericardium was not closed by suture. Moreover, the
magnitude of ventricular interaction, in which the
percent reduction in ventricular volume after an
increase in the opposite ventricular pressure tended
to be greater in the LV without the pericardium,
was also demonstrated in the LV with the pericardium intact (Fig. 6). Janicki and Weber (1980b) had
similar findings and showed the important role of
the pericardium in ventricular interactions. From
the data demonstated in Table 5-(2), we can also
explain our findings as follows, the larger the distension of the heart, which was induced by increased numbers of distended heart chambers, or
by a larger magnitude of increased filling pressure,
the greater the effect of mechanical interaction by
moving on to further steep parts of the pericardial
P-V curve. This possibility is also supported by the
following results, i.e., two additional experiments,
in which LV P-V curves were measured while volumes of other heart chambers were clamped and
did not change during the measurements of P-V
curves, strongly indicated a mechanical interaction
of the heart chambers, although this situation does
not occur in situ. Similarly, the smaller effect of the
atrial pressure compared with that induced by an
increase in the opposite ventricular pressure on
ventricular P-V relationship is considered to be
dependent on the smaller amount of volume occupied by the atrium in the pericardial sac, even if the
atrial pressure increased to the same magnitude.
Thus, when we take these three factors into account, i.e., the pericardium, the atrial pressure, and
the opposite ventricular pressure for the shift in the
p(v) function with the fourth order polynomial, the
contribution of each factor should be noted [Table
In summary, we intended to investigate the mechanical interaction of four heart chambers and the
magnitude of the shift in the entire p(v) function
during various interventions. As a result, we showed
the direct mechanical effect of atrial pressure on
the ventricular P-V relationship, which has been
suggested by others (Tyberg et al, 1978; Ross,
1979). Furthermore, the effect became dramatically
99
greater, when an increase of atrial filling pressure
occurred, simultaneous with an increase of ventricular filling pressure. We demonstrated that the
pericardium played an important role in such mechanical interactions.
Finally, the pericardium has considerably capacity for expansion in chronic cardiac dilatation (Hort
and Braun, 1962) and shows plastic deformation
with repeated distensions (Morgan, 1965). Thus, it
is impossible to generalize the results of our acute
animal experiments to chronic diseased hearts.
Therefore, we should be careful of the direct clinical
application of our present results. However, when
filling pressures of heart chambers increase concomitantly in heart diseases such as heart failure,
ventricular diastolic pressure may be a misleading
index of the ventricular volume and, moreover, we
consider the decreased ventricular function may be
partly due to this decreased ventricular compliance
via the Frank-Starling mechanism.
Acknowledgments
We are grateful to Hiroyuki Uchiyama of Tanabe Seiyaku
Co. Ltd. for his excellent statistical advice regarding this manuscript. We also wish to thank Ronald R. Bankson for advice
about English usage.
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Y Maruyama, K Ashikawa, S Isoyama, H Kanatsuka, E Ino-Oka and T Takishima
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Circ Res. 1982;50:86-100
doi: 10.1161/01.RES.50.1.86
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