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Am J Physiol Heart Circ Physiol 272: H2679-H2685, 1997;
0363-6135/97 $5.00
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AJP - Heart and Circulatory Physiology, Vol 272, Issue 6 2679-H2685, Copyright © 1997 by American Physiological Society


ARTICLES

Cytosolic [Ca2+], [Na+], and pH in guinea pig ventricular myocytes exposed to anoxia and reoxygenation

L. Ralenkotter, C. Dales, T. J. Delcamp and R. W. Hadley
Department of Pharmacology, University of Kentucky College of Medicine, Lexington 40536-0084, USA.

The aim of this study was to evaluate whether the magnitude and time course of the intracellular acidification observed in anoxic cardiac myocytes was sufficient to protect against reoxygenation-induced hypercontracture. Cytosolic [Ca2+], [Na+], and pH were measured using fluorescent indicators in myocytes that were first subjected to both anoxia and glucose deprivation and then oxygen and glucose restoration 15-30 min after the onset of rigor. The cytosol underwent a profound acidification early in anoxia (pH 7.21 to 6.84) that reached a plateau at the time of rigor contracture. In contrast, [Na+] rose throughout anoxia. Cytosolic [Ca2+] underwent little rise during anoxia, but reoxygenation induced a large spike in [Ca2+]. Reoxygenation also induced a significant secondary acidification of the cytosol that was apparently induced by the spike in [Ca2+]. The characteristics of this secondary acidification were deemed sufficient to provide partial protection against the hypercontracture associated with the reoxygenation-induced [Ca2+] transient.


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