Effects of Acute Increases in Left Ventricular Preload on Indices of Myocardial Function in Conscious, Unrestrained and Intact, Tranquilized Baboons

Abstract

A B S T R A C T 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 dPldtmar and the maximum velocity of myocardial fiber shortening (LV dD/ dtmax) did not change. Volume loading afterf/-adrenergic or combined 3-adrenergic and cholinergic blockades or volume loading with blood instead of saline also failed to augment LV dP/dt max and LV dDIdt 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

Semi‐mechanistic modelling platform to assess cardiac contractility and haemodynamics in preclinical cardiovascular safety profiling of new molecular entities

“…10% variation in the signal. These findings are consistent with earlier reports that show a moderate effect of preload on contractility (Zimpfer & Vatner, 1981).…”

“…Our results show that dPdt max is moderately affected by preload as it accounts for up to 10% variation in the signal. These findings are consistent with earlier reports that show a moderate effect of preload on contractility (Zimpfer & Vatner, 1981).…”

A 1 Adenosine Receptor Upregulation Accompanies Decreasing Myocardial Adenosine Levels in Mice With Left Ventricular Dysfunction

“…Most likely, the increase in arterial pressure and sympathetic activation caused the transient augmentation of dP/dt. 37,38 Because TNF 1.6 responded to A 1 -AR agonists differently than WT mice, the effects of A 1 -AR agonists on heart rate and hemodynamics may be dependent on the mode of administration, experimental system, and physiological state of the myocardium. It should be noted that Liao et al 39 showed that A 1 -AR agonists delivered regularly via minipump attenuated cardiac hypertrophy and prevented heart failure in mice with LV pressure overload but had no effect on heart rate.…”

Echocardiographic assessment of systolic and diastolic left ventricular function using an automatic boundary detection system

“…In patients with normal left ventricular function, the FACapical 4 chamber and FACmean correlated positively with the LVEDP, however there was no correlation between EF and LVEDP. Whilst in patients with abnormal ventricular function both the FAC (all views) and the EF correlated negatively with the LVEDE These findings possibly simply confirm that in normal hearts LVEDP mainly reflects preload [16] and that moderate changes in preload although have little effect in the EF [17,18] affect in a much sensitive way the FAC. However although it would be interesting to postulate that the positive correlation found between ventricular filling pressures and FAC reflects operation of the Frank-Starling principle [19] the only way for this to be proven would have been to obtain data from the same heart.…”