End-systolic pressure-volume relationship and intracellular control
of contraction.
Landesberg, Amir.
Heart System Research Center, The Julius Silver Institute,
Department of Biomedical Engineering, Technion-Israel Institute of
Technology
APStracts 2:0322H, 1995.
The left ventricle (LV) pressure-volume relationship and the effect of
ejection on pressure generation are predicted theoretically based on
the intracellular control mechanisms. The control of contraction is
described based on coupling calcium kinetics and crossbridge cycling.
The analysis of published skinned and intact cardiac muscle data
suggests two feedback control loops: a) A positive cooperative
mechanism which determines the force-length relationship, the length
dependence calcium sensitivity of the contractile filaments and the
related Frank Starling Law. b) A negative mechanical feedback, which
determines the force-velocity relationship and the generated power.
The interplay between these two feedback mechanisms explains the wide
spectrum of phenomena associated with the end-systolic pressure
-volume relationship (ESPVR); it provides an explanation to the
"shortening deactivation" and to the recent observations of
the positive effect of ejection on the ESPVR, i.e., the increase of
the end-systolic pressure of the ejecting beat over the pressure of
the isovolumic beat at the same end-systolic volume. Furthermore, the
analysis suggests that the LV contractility depends on the balance
between the two intracellular mechanisms and that the effect of
loading conditions is determined through these intracellular
mechanisms.
Received 22 November 1994; accepted in final form 19 July 1995.
APS Manuscript Number H1039-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 August 1995.