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Intermittent hypoxia has been shown to provide myocardial protection against ishemia/reperfusion-induced injury. Cardiac myocyte loss through apoptosis has been reported in ischemia/reperfusion injury. Our aim was to investigate whether intermittent hypoxia could attenuate ischemia/reperfusion-induced apoptosis in cardiac myocytes and its potential mechanisms. Adult male Sprague-Dawley rats were exposed to hypoxia simulated 5000 m in a hypobaric chamber for 6 h/day, lasting 42 days. Normoxia group rats were kept under normoxic conditions. Isolated perfused hearts from both groups were subjected to 30 min of global ischemia followed by 60 min reperfusion. Incidence of apoptosis in cardiac myocytes was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) and DNA agarose gel electrophoresis. Expressions of apoptosis related proteins, Bax and Bcl-2, in cytosolic and membrane fraction were detected by Western Blotting. After ischemia/reperfusion, enhanced recovery of ca
Intermittent hypoxia has been shown to provide myocardial protection against ishemia / reperfusion-induced injury. Cardiac myocyte loss through apoptosis has been reported in ischemia / reperfusion injury. Our aim was to investigate whether intermittent hypoxia could attenuate ischemia / reperfusion-induced apoptosis in cardiac myocytes and male female Sprague-Dawley rats were exposed to hypoxia simulated 5000 m in a hypobaric chamber for 6 h / day, lasting 42 days. Normoxia group rats were kept under normoxic conditions. Incidence of apoptosis in cardiac myocytes was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) and DNA agarose gel electrophoresis. Expressions of apoptosis related proteins, Bax and Bcl-2, in cytosolic and membrane fractions were detected by Western Blotting. After ischemia / reperfusion, enhan ced recovery of ca