Length dependence of activation studied in the isovolumic blood-perfused dog heart.

Abstract

SUMMARY. In studies utilizing the isolated isovolumic blood-perfused canine heart, left ventricular pressure was measured following a sudden expansion of ventricular volume. An increase in performance occurred in two phases: first, there was an instantaneous rise of developed pressure simultaneous with ventricular distension; in the second phase, developed pressure continued to increase for several minutes until a final steady state was reached. The immediate increase in developed pressure occurred with a prolongation of the time-to-peak pressure, and there was no further change of time-to-peak pressure during the time-dependent increase of developed pressure. In another series of experiments, systolic pressure was elevated without changing resting volume, and mechanical performance changed in a different manner: after an increase in systolic load, there was a modest and transient decrease of developed pressure; thereafter, ventricular pressure recovered only to original values. The influence of different degrees of ventricular expansion, calcium, and verapamil were studied. Under higher ventricular dilations the immediate as well as the slow increase of contraction were heightened and the time to reach half of the slow increase was shortened. When ventricular dilation was induced during an infusion of calcium chloride, higher values for the immediate pressure increase were observed, whereas the timedependent increase and the time to reach half of the slow increase did not change in comparison with control studies. Verapamil decreased the immediate and the time-dependent enhancement of contraction. The time-dependent increase in developed pressure occurs more slowly with verapamil. These findings in the intact heart are in accord with the hypothesis that myocardial stretch is followed by an increase in intracellular calcium stores, and with the concept that the Frank-Starling mechanism involves an activation of the contractile state. (Circ Res 55: 59-66, 1984)

<b>Coenzyme Q</b>₁₀<b> Exogenous Administration Attenuates Cold Stress Cardiac Injury</b>

“…These results indicate that, even though contractile capacity was depressed at all levels of myofiber lengthening, profound cold stress did not affect length dependent activation, which bases the Frank-Starling mechanism. [26][27][28] This seems to be a dysfunction consequent to impairment of maximum calcium-activated force rather than a decrease of myofilament calcium sensitivity. 29) Aside from systolic function impairment, rat hearts of the P group disclosed ultrastructural features that documented the profound cold stress cardiac injury.…”

Dual role of endothelin-1 via ETA and ETB receptors in regulation of cardiac contractile function in mice

“…Initially, there is a very rapid increase in contractile force, which is followed by the slow force response (the Anrep effect) during the next minutes, accounting for ϳ20% of the whole contractile response (34,35). During the initial minutes of myocyte stretch, a number of autocrine/paracrine factors are released, contributing to activation of various intracellular signaling mechanisms (18,34).…”

Mechanoelectrical feedback: independent role of preload and contractility in modulation of canine ventricular excitability.

“…However, diastolic volume and inotropic state may not be independent determinants of myocardial performance in that developed tension at a given muscle length is dependent on the degree of activation of the contractile system and conversely, activation of the contractile system depends on resting muscle length (length-dependent activation) (44,45). Length-dependent activation has also been shown to be operative in the intact ventricle (46). Therefore, increased preload and contractility may exert their similar effects on excitability and action potential duration through a common cellular mechanism.…”