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Am J Physiol Heart Circ Physiol (December 6, 2001). doi:10.1152/ajpheart.00464.2001
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Articles in PresS, published online ahead of print December 6, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00464.2001
Submitted on May 30, 2001
Accepted on November 29, 2001

Phase I and Phase II of Short-Term Mechanical Restitution in Perfused Rat Left Ventricles

Cristian Dumitrescu1, Prakash Narayan1, Yuanna Cheng2, Igor R Efimov2, and Ruth A Altschuld1*

1 Biophysics Program and Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA
2 Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA

* To whom correspondence should be addressed. E-mail: altschuld.2{at}osu.edu.

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 msec following a steady state beat (F0) in perfused rat ventricles paced at 2 or 3 Hz. Plots of F1/F0 vs the extrasystolic interval consisted of 2 phases, phase I, which occurred prior to 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 (-) 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+.




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