Phase I and phase II of short-term mechanical restitution in perfused rat left
ventricles.
Dumitrescu, Cristian, Prakash Narayan, Yuanna Cheng, Igor R. Efimov, and Ruth A.
Altschuld.
1The Ohio State University Biophysics Program and Dorothy M. Davis Heart and
Lung Research Institute, Columbus, 43210; 2The Cleveland Clinic Foundation,
Department of Cardiology, Cleveland, Ohio 44195
APStracts 8:0601H, 2001.
We examined the contributions of the Ca2+ channels of the sarcolemma and of the
sarcoplasmic reticulum to electromechanical restitution. Extrasystoles (F1) were
interpolated 40-600 ms following a steady-state beat (F0) in perfused rat ventricles paced
at 2 or 3 Hz. Plots of F1/F0 versus the extrasystolic interval consisted of phase I, which
occurred before relaxation of the steady-state beat, and phase II, which occurred later.
Phase I exhibited a period of enhanced left ventricular pressure development that
coincided with action potential prolongation. Phase I was eliminated by «minus»BAY K
8644 (100 nM) and FPL 64176 (150 nM), augmented by 3 µM thapsigargin plus 200 nM
ryanodine and unaffected by KN-93 and KB-R7943. Phase II was accelerated by the
Ca2+ channel agonists and by isoproterenol but was eliminated by thapsigargin plus
ryanodine. The results suggest that phase I of electromechanical restitution is caused by a
transient L-type Ca2+ current facilitation, whereas phase II represents the recovery of the
ability of the sarcoplasmic reticulum to release Ca2+.
Received 30 May 2001; accepted in final form 29 November 2001
APS Manuscript Number H464-1.
Article publication pending Am J Physiol Heart Circ Physiol
ISSN 1080-4757 Copyright 2001 The American Physiological Society.
Published in APStracts on 26 December 2001