Preload does not affect relaxation rate in normal, hypoxic, or hypertrophic myocardium

Abstract

To determine whether isolated changes in preload (end-diastolic force) can influence myocardial relaxation rate in normal or abnormal (hypoxic or hypertrophic) hearts, isolated LV papillary muscles from normal Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats were studied using physiologically sequenced contractions. While total (systolic) load and late (lengthening) load were held constant, maximum isometric force decline (peak -dT/dt) and maximum isotonic lengthening rate (peak +dL/dt) were measured at seven levels of preload that varied from 115 to 55% of the resting tension at maximum length-tension curves (Lmax). Muscles from normal rats were studied in the oxygenated state (95% O2-5% CO2) and in the hypoxic state (95% N2-5% CO2). Preload did not effect peak -dT/dt or peak +dL/dt in either oxygenated or hypoxic muscles. During hypoxia, peak -dT/dt and peak +dL/dt were 9.5 +/- 1.0 g.mm-2.s-1 and 0.3 +/- 0.1 muscle length/s, respectively, at a preload of 115% compared with 9.0 +/- 1.2 g.mm-2.s-1 and 0.2 +/- 0.1 at a preload of 55%. In separate experiments, the effect of preload on relaxation rate was studied in WKY and SHR rats. In neither group did preload have an independent effect on relaxation rate. In the SHRs, peak -dT/dt and peak +dL/dt were 24.3 +/- 5.3 g.mm-2.s-1 and 0.7 +/- 0.1 muscle length/s, respectively, at a preload of 115% compared with 24.7 +/- 6.6 and 0.8 +/- 0.1 at a preload of 55%. Thus, in hypoxic and hypertrophic myocardium, as in normal muscle, an acute isolated change in preload did not influence the rate of force decline or muscle lengthening.

Effects of lisinopril on experimental ischemia in rats. Influence of infarct size

“…In such situations, the systolic pressure (SP) developed during the contractions and the +dp/dt Have Been accepted as parameters of systolic function [11][12][13] . In the same way, -dp/dt has been used as a parameter of diastolic function 14 .…”

Multivariate regression analysis of the influence of aortic pressure, end—diastolic pressure, and heart rate on left ventricular relaxation in isolated ejecting rat and guinea pig hearts

“…It may be surmised from a further unpublished observation we have made that increasing LVEDP diminishes τ at small LVEDP but increases it rapidly at very high LVEDP, whereas τ is only slightly affected in a range of moderate LVEDP, such as in the present protocol. In hypoxic or hypertrophic rat myocardium, preload also has not affected the relaxation rate considerably [27].…”

“…In other studies reporting prolonged τ when LVEDP was increased, LVP max was not kept constant but also allowed to increase [4 (protocol B), 7,16]. Experimental methods to manipulate LVEDP and to calculate τ that are different from that presently adopted showed no or almost insignificant lusitropic LVEDP effects in dogs, rabbits, and humans [9,21,24,27].…”

Load as an acute determinant of end-diastolic pressure-volume relation

“…Afterload elevations exceeding the relative load of the transition (80, 90, and 100% interventions) progressively slowed the rate of LVP fall, with the amount of slowing increasing from low to mid preload but not changing from mid to high preload. Previous studies reported contradictory effects of preload on rate of LVP fall, with some authors describing a decrease in relaxation rate (5,9,29,36) and others describing no effects (35,39) in response to preload elevations. Some of these discrepancies were attributed to the concomitant changes in preload and afterload in response to the majority of interventions used to modify preload (e.g., volume infusion and caval occlusions).…”