Volume loading slows left ventricular isovolumic relaxation rate. Evidence of load-dependent relaxation in the intact dog heart.

Abstract

SUMMARY We studied the effects of volume loading on left ventricular isovolumic relaxation rate in 16 intact anesthetized dogs. End-diastolic pressure, mean aortic systolic pressure, dp/dt mnx , and heart rate were measured at end expiration and end inspiration. Volume loading to approximately 5, 10, 15, and 20 mm Hg above initial end-diastolic pressure was performed. In nine dogs, simultaneous ventricular dimensions were measured with previously implanted tantalum screws using biplane cineangiography. Similar volume loading was done in open-chest and open-pericardium states. Relaxation rate was measured in 3413 beats using T, the time constant of exponential isovolumic pressure fall. T was calculated as reported previously by others and also from a linear regression of dp/dt against p, to eliminate the effects of extracavity pressure changes. T always increased significantly with volume loading, indicating slower relaxation. (For example, with the chest intact, mean T increased from 26 ± 2 (SEM) msec before volume loading to 41.5 ± 4 msec after volume loading.) Using multiple linear regression analysis, we found, in agreement with previous reports, that T decreased significantly as dp/dt,,., and heart rate increased. In contrast to previous reports, we also found that T increased significantly as end-diastolic and mean aortic systolic pressure increased. These four variables taken together accurately predicted T [SEE (standard error of estimate) = 3.2 msec, R = 0.94, P < 0.001]. Geometric variables, including ventricular dimensions and ejection fraction, did not have a statistically significant effect on T independent of the hemodynamic variables. Opening the chest or pericardium did not have a consistent effect on T. Volume loading slows isovolumic relaxation rate in the intact canine heart. This effect appears to be a reflection of the dependence of relaxation on both end-diastolic and mean aortic systolic pressures. Circ Res 48: [813][814][815][816][817][818][819][820][821][822][823][824] 1981 STUDIES of the hemodynamic determinants of left ventricular isovolumic relaxation grew out of interest in the effects of ischemia on diastolic pressure. Following the observation of Barry et al. (1974) that left ventricular diastolic pressure increased without significant increases in end-diastolic volume during angina pectoris, McLaurin et al. (1973) investigated the hypothesis, first suggested by Mitchell et al. (1960), that incomplete relaxtion during diastole might cause an apparent acute stiffening of the left ventricle on the next beat. McLaurin et al. (1973) observed that angina produced a significant decrease in the magnitude of dp/dtmin (also called -dp/dtmax) and suggested that this response indicated impaired relaxation. However, the interpretation of this and similar clinical studies (Papapietro et al., 1979) is clouded by the complex interaction of many changes that occur during ischemia, including depressed inotropic state, increased preload, and increased afterload. Studies of the determinants of dp/d...

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