Reducing left ventricular volume to zero in isolated rabbit hearts caused a 5.7% decrease in right ventricular developed pressure (P<0.001), with further decreases upon coronary ligation and free wall cutting.
Right ventricular function (n=10)
Reducing LV volume, coronary ligation, and cutting LV free wall vs Baseline optimal LV volume
Right ventricular developed pressure (RVDP), p=<0.001
p-value: p=<0.001
The possibility that left ventricular (LV) performance might affect right ventricular (RV) function through the myocardium was examined by using isolated, flow-perfused, paced rabbit hearts beating isovolumically. Reducing LV volume from its optimal volume to zero caused a 5.7% decrease (N = 10, P less than 0.001) in right ventricular developed pressure (RVDP). Ligating the anterior ventricular branches of the left coronary artery which in the rabbit supply the LV free wall resulted in an additional 9.3% decrease in RVDP (N = 5, P = 0.05) within 3 min of ligation. Finally, cutting the LV free wall from the atrioventricular orifice to the apex (thereby preventing any developed LV free wall force during systole) caused a 45% further decrease in RVDP (N = 2, P less than 0.02). Cineradiographic study showed that the alterations in RVDP resulting from changes in LV volume and coronary occlusion correlated significantly (N = 5, P less than 0.01) with the magnitude of septal bulging into the RV cavity during systole. The results indicate that alteration in LV free wall function and changes in LV volume can directly effect RVDP through the myocardium.
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Santamore et al. (Wed,) conducted a other in Right ventricular function (n=10). Reducing LV volume, coronary ligation, and cutting LV free wall vs. Baseline optimal LV volume was evaluated on Right ventricular developed pressure (RVDP) (p=<0.001). Reducing left ventricular volume to zero in isolated rabbit hearts caused a 5.7% decrease in right ventricular developed pressure (P<0.001), with further decreases upon coronary ligation and free wall cutting.
synapsesocial.com/papers/6a09064729af591ab7017293 — DOI: https://doi.org/10.1152/jappl.1976.41.6.925
William P. Santamore
Rutgers, The State University of New Jersey
Peter R. Lynch
Western University
J. L. Heckman
Temple University
Journal of Applied Physiology
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