A. Landesberg, END-SYSTOLIC PRESSURE-VOLUME RELATIONSHIP AND INTRACELLULAR CONTROL OF CONTRACTION, American journal of physiology. Heart and circulatory physiology, 39(1), 1996, pp. 338-349
The left ventricular (LV) pressure-volume relationship and the effect
of ejection on pressure generation are predicted theoretically based o
n the intracellular control mechanisms. The control of contraction is
described based on coupling calcium kinetics and cross-bridge cycling.
The analysis of published skinned and intact cardiac muscle data sugg
ests two feedback control loops: 1) a positive cooperative mechanism t
hat determines the force-length relationship, the length dependence ca
lcium sensitivity of the contractile filaments, and the related Frank
Starling law; and 2) a negative mechanical feedback. that determines t
he force-velocity relationship and the generated power. The interplay
between these two feedback mechanisms explains the wide spectrum of ph
enomena associated with the end-systolic pressure-volume relationship
(ESPVR); it provides an explanation for the ''shortening deactivation'
' and for the recent observations of the positive effect of ejection o
n the ESPVR, i.e,, the increase of the end-systolic pressure of the ej
ecting beat over the pressure of the isovolumic beat at the same end-s
ystolic volume. Furthermore, the analysis suggests that the LV contrac
tility depends on the balance between the two intracellular mechanisms
and that the effect of loading conditions is determined through these
intracellular mechanisms.