Abstract
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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