Cardiac end-diastolic dilation during acute blood pressure elevation is inotropy dependent.

To examine if the degree of left ventricular (LV) end-diastolic dilation during an acute blood pressure elevation is inotropy dependent, the descending thoracic aorta was occluded before and during a continuous isoproterenol infusion into the left coronary artery in 10 open-chest pigs. The increase in peak LV systolic pressure and in LV tension-time-index induced by aortic occlusion, were equal before and during the isoproterenol infusion. Left and right ventricular (RV) segment lengths were continuously recorded in the free walls of both ventricles, by an ultrasonic technique. A slight fall in LV end-diastolic segment length by the intracoronary isoproterenol infusion was corrected by an i.v. saline infusion. Left ventricular end-diastolic volume was therefore equal at both levels of inotropy when the aorta was occluded, and the heart rate was kept constant by right atrial pacing. At control inotropy, aortic occlusion induced a rise in LV end-diastolic segment length; 6.0 (4.0-8.2)% (median and 95% confidence interval), compared with the smaller (P less than 0.05) increase of 3.8 (2.6-5.5)% during isoproterenol infusion. The end-systolic segment length increased more (P less than 0.01) at control inotropy than during intracoronary isoproterenol infusion: 10.9 (6.9-14.4)% and 4.1 (1.5-7.4)%, respectively. In the RV, both end-diastolic and end-systolic segment length increased slightly during aortic occlusion but only at control inotropy. Thus during an acute blood pressure elevation, the end-diastolic and end-systolic ventricular volumes are better maintained at high than at control inotropy.