The effects of acute volume loading were examined on indices of left ventricular (LV) function in conscious, unrestrained and intact, tranquilized baboons. Experiments were conducted 1-3 mo after implantation of ultrasonic transducers to measure LV internal diameter and wall thickness, and miniature LV pressure gauges and aortic and left atrial catheters. In 10 intact, tranquilized baboons, rapid volume loading with saline increased LV end-diastolic pressure by 23.7±2.6 mm Hg, LV end-diastolic diameter by 7.8±1.5%, LV stroke work by 37.5±7.8%, while mean arterial pressure and peak LV wall stress did not change significantly. Despite the increase in preload and activation of the Frank-Starling mechanism, LV dP/dt(max) and the maximum velocity of myocardial fiber shortening (LV dD/dt(max)) did not change. Volume loading after β-adrenergic or combined β-adrenergic and cholinergic blockades or volume loading with blood instead of saline also failed to augment LV dP/dt(max) and LVdD/dt(max) despite the increase in preload. In order to volume load the baboons in the conscious state, a radiofrequency (RF) interrogator system was devised, which upon receipt of a radio command, activated a battery operated pump to infuse 1,000 ml of saline i.v. to the baboons. In these experiments, preload rose, i.e., LV end-diastolic diameter increased by 13.9±2.1% and the Frank-Starling mechanism could be demonstrated i.e., stroke work rose by 42.8±7.4%, but LVdP/dt(max) did not change. After preload was depressed by hemorrhage, the rapid infusion of either blood or saline increased LV by dP/dt(max) by 92.7±18.5% and LV dD/dt(max) by 64.3±10.1%. Thus, acute volume loading in the conscious baboons increased LV end-diastolic size and even stroke work substantially. However, preload dependency of LV dP/dt(max) and the maximum velocity of myocardial fiber shortening was only encountered at low levels of LV preload.
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