The pH paradox in ischemia-reperfusion injury to cardiac myocytes
作者： J. J. Lemasters , J. M. Bond , E. Chacon , I. S. Harper , S. H. Kaplan
DOI: 10.1007/978-3-0348-8988-9_7
关键词:
摘要: During myocardial ischemia, a large reduction of tissue pH develops, and returns to normal after reperfusion. In recent studies, we evaluated the role in ischemia/reperfusion injury cultured cardiac myocytes perfused papillary muscles. Acidosis (pH ≤ 7.0) protected profoundly against cell death during ischemia. However, return from acidotic reperfusion caused lose viability. This worsening is ‘pH paradox’ was mediated by changes intracellular (pHi), since manipulations that pHi increase more rapidly accelerated killing, whereas delayed prevented loss myocyte Specifically, inhibition Na+/H+ exchanger with dimethylamiloride or HOE694 physiologic reperfusion-induced killing both muscle. Dimethylamiloride HOE 694 did not reduce free Ca2+ By contrast, dichlorobenzamil, an inhibitor Na+/Ca2+ exchange, decreased but killing. Thus, paradox Ca2+-dependent.
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