Rapid in vivo determinations of instantaneous right ventricular pressure and volume in dogs

Schwiep, Frances; Cassidy, S. S.; Ramanathan, Murugappan; Johnson, Robert L.

doi:10.1152/ajpheart.1988.254.4.h622

Cited by 7 publications

(14 citation statements)

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“…The ventricular pressure-area loop was not rectangular and was similar to the shape of the mature right ventricle (24,25). The finding that isovolumetric contraction and relaxation phases were short was somewhat different from that of Keller et al (17), who found that there were definite isovolumetric phases during a cardiac cycle in the chick embryonic ventricle.…”

Section: Discussioncontrasting

confidence: 62%

Hemodynamics and Ventricular Function in the Day-12 Rat Embryo: Basic Characteristics and the Responses to Cardiovascular Drugs

et al. 1995

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We investigated the basic characteristics of the rat embryonic circulation and also looked at the hemodynamic effects of a-and P-agonists, digitalis, and atrial natriuretic peptide, using a modified organ culture system in which the embryo was placed in oxygenated Hanks' balanced salt solution, blood pressure was measured by a servo-null micropressure system, and blood flow pattern was obtained by a 20-MHz pulsed Doppler velocity meter. The peak pressure was 0.5 ? 0.04 (SEM) mm Hg at the atrium (n = 6), 2.3 + 0.10 mm Hg at the ventricle (n = 15), 1.6 ? 0.03 mm Hg at the truncus (n = 7), and 1.0 ? 0.05 mm Hg at the umbilical artery (n = 21). There was a pressure drop from the I ventricle to the truncus and then a smaller pressure decrease to I the umbilical artery. The atrial a-wave was 20% of ventricular I pressure and ventricular inflow blood flow pattern showed very low early-to-late filling ratio, indicating that the ventricle was stiff. These findings were essentially the same as in the chick embryo. We recorded the ventricular image by using a highspeed video system with a frame rate of 200/s, and the ventricular pressure-area loop showed a triangular shape with short isovolumetric phases, which was different from that of the chick embryo at a similar stage. Isoproterenol increased ventricular pressure from 2.3 ? 0.1 to 2.6 2 0.1 mm Hg (n = 7, p < 0.05) and decreased umbilical blood pressure from 0.68 -C 0.05 to 0.61 + 0.04 mm Hg (n = 7, p < 0.05), suggesting contraction of the outflow tract, although positive change in pressure per unit time of ventricular pressure did not change. Ventricular negative change in pressure per unit time was increased with isoproterenol from 40 + 4 to 51 + 6 mm Hg/s (n = 7, p < 0.05), implicating improvement of diastolic function. Atrial natriuretic peptide and norepinephrine did not exert any significant responses, which was in contrast to the marked effects of these drugs seen in chick embryos. Acetylstrophanthidin, a rapid-acting digitalis, slowed the heart rate from 184 + 4 to 171 t 3 bpm (n = 6, p < 0.05) but did not change other parameters. In conclusion, basic characteristics of the circulation of the mammalian embryo are similar to those of the avian embryo, but responses to various cardiovascular agents known in the chick embryo cannot be extrapolated to the mammalian embryo. Previous studies have shown that basic cardiovascular function becomes established at very early stages of cardiovascular morphogenesis and the embryonic circulation is crucial to ensure normal organogenesis (1-3). The critical role of the embryonic circulation was shown by studies in which altered hemodynamics had adverse effects on the normal growth of the embryo (4-6); thus, stability of embryonic circulation is very important for the normal development and growth of the embryo. Inasmuch as the heart and vessels are not innervated during the early and critically important period of organogen-

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Section: Discussioncontrasting

confidence: 62%

Hemodynamics and Ventricular Function in the Day-12 Rat Embryo: Basic Characteristics and the Responses to Cardiovascular Drugs

et al. 1995

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“…In situ heart 25 RV-Ee, was reported to be 4.14 mm Hg/ml; this value, which was obtained by altering afterload, may be overestimated and somewhat incorrect, 32 although few investigators have examined the effect of afterload on RV-ESPVR. RV-E^ (mean value in small LV volume level, 2.63 mm Hg/ml) in our study is somewhat higher than that in the study of Maughan et al 24 and lower than that of Schwiep et al 25 RV-V 0 (3.92 ml [or 5.92 ml when the 2-ml volume of the balloon wall and hardware was included]) in our study is lower than that of Maughan et al There may be a limitation in our study because we used defibrillated hearts. However, our value of RV-E a was within the physiological range, as found in the previous studies.…”

Section: Discussioncontrasting

confidence: 77%

“…This phenomenon is considered to contribute, at least partly, to the changes in RV-E« and RV-V 0 ( Figure 6). Recently, several authors have investigated RV-ESPVR in isolated dog heart, 1724 in situ dog heart, 25 and human heart. 26 - 28 Maughan et al 24 reported that RV-ESPVR was linear and sensitive to change in the contractile state, as reported for LV-ESPVR.…”

Section: Discussionmentioning

confidence: 99%

Effect of left ventricular volume on right ventricular end-systolic pressure-volume relation. Resetting of regional preload in right ventricular free wall.

Yamaguchi

Tsuiki

Mikami

et al. 1989

Circulation Research

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Effect of left ventricular (LV) volume on right ventricular (RV) end-systolic pressure-volume relation (ESPVR) was investigated, and the mechanism was examined from a standpoint of the alteration of RV free wall mean fiber length. Twelve cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were controlled independently were used, and RV-ESPVR was determined at three different LV volume levels. At small (10.2 +/- 0.6 ml), middle (15.3 +/- 1.0 ml), and large (20.5 +/- 1.4 ml) LV volume, the slope of the RV-ESPVR was 2.63 +/- 0.13, 2.74 +/- 0.13, and 2.89 +/- 0.12 mm Hg/ml, respectively, and each value was significantly different from the others (p less than 0.01). The volume intercept (V0) of the relation (RV-V0) was significantly decreased with the increment of LV volume (RV-V0 in small, middle, and large LV volume; 3.92 +/- 0.68, 3.39 +/- 0.67, and 2.87 +/- 0.71 ml, respectively; p less than 0.01). In nine hearts, RV free wall lengths in latitudinal and meridional direction were measured at three LV volume levels when RV volume was held constant (16.1 +/- 1.1 ml). RV latitudinal end-diastolic length was significantly augmented with increasing LV volume (latitudinal length in small, middle, and large LV volume; 9.68 +/- 0.55, 9.81 +/- 0.56, and 9.92 +/- 0.55 mm, respectively). RV meridional end-diastolic length also increased significantly with increasing LV volume.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…The preparation used for this study was an anaesthetized, open-chest, this technique for the rabbit RV (Schwiep et al, 1988) and others for the LV (Baan et al, 1984), it is not clear whether animals with larger sized hearts would behave in a similarmanner. Potentially, these young animals might have residual neonatal RV hypertrophy, which might cause them to behave differently.…”

Section: Limitations Of the Studymentioning

confidence: 99%

Dynamic right and left ventricular interactions in the pig

Pinsky

2020

Experimental Physiology

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I characterized the dynamic factors determining ventricular interdependence with and without the pericardium. I measured right (RV) and left ventricular (LV) pressures and volumes simultaneously using conductance catheters in seven pentobarbitoneanaesthetized open-chested 5-to 7-week-old piglets. I studied these effects during apnoea, inferior vena caval occlusion and rapid partial aortic and pulmonary arterial occlusions. Conductance catheter-defined long-axis regional volumes were assessed to define regional contractile synchrony. Closed-pericardium measures were made from an initial (baseline) volume, then after two 20 ml kg −1 fluid loads followed by an open-pericardium step. Baseline RV and LV volumes were similar. Aortic occlusion increased LV pressures and volumes and RV end-systolic pressure such that RV endsystolic elastance increased without changes in RV contraction synchrony, not affected by the pericardium. Pulmonary artery occlusion increased RV end-systolic pressure but not end-systolic volume. On the subsequent beat, RV end-diastolic pressure increased, whereas LV end-diastolic volume and diastolic compliance decreased. These effects were attenuated by opening the pericardium. Contraction synchrony across longitudinal segments was unaltered by either aortic or pulmonary artery occlusion. I conclude that the determinants of systolic and diastolic ventricular interdependence are different. Increasing RV pressures causes diastolic RV-to-LV interdependence, decreasing LV diastolic compliance and dependent on an intact pericardium. An increase in LV end-systolic pressure increases RV end-systolic elastance independent of the pericardium and has a minimal effect on RV diastolic function or contraction synchrony.

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Rapid in vivo determinations of instantaneous right ventricular pressure and volume in dogs

Cited by 7 publications

References 0 publications

Hemodynamics and Ventricular Function in the Day-12 Rat Embryo: Basic Characteristics and the Responses to Cardiovascular Drugs

Hemodynamics and Ventricular Function in the Day-12 Rat Embryo: Basic Characteristics and the Responses to Cardiovascular Drugs

Effect of left ventricular volume on right ventricular end-systolic pressure-volume relation. Resetting of regional preload in right ventricular free wall.

Dynamic right and left ventricular interactions in the pig

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