Hypoxia-reoxygenation induced apoptosis of cardiomyocytes and the effect of nitric oxide

AIM To study hypoxia reoxygenation induced apoptosis of neonatal rat cardiomyocytes and the roles of nitric oxide in this process. METHODS Cultured neonatal rat cardiomyocytes were divided into two groups. Cells of one group were cultured in an incubator of 950 mL·L -1 N 2 and 50 mL·L -1 CO 2 for 16 h, 32 h and 48 h followed by normal incubation for 6h to form the cell model of hypoxia reoxygenation injury.Cells of another group were cultured in the same hypoxia condition for 16 h, 32 h and 48 h. Before they were put in normal condition for 6 h, NO donor SNAP was added to the media to form the final concentration of 100 μmol·L -1 . Apoptosis was detected by TUNEL and flow cytometer. RESULTS Apoptotic cells were detected by TUNEL after hypoxia of 16 h, 32 h and 48 h followed by 6 h reoxygenation and the apoptotic rates of cardiomyocytes were (5 5±0 7)%, (11 0±1 1)% and (14 2±1 6)% respectively detectedby flow cytometer. The apoptotic rates of myocardiums with SNAP were (3 2±0 7)%, (7 8±0 7)% and (10 9±1 0)% respsctively. CONCLUSION The apoptotic rates of cardiomyocytes undergoing hypoxia reoxygenation injury increase with time of hypoxia; NO can inhibit apoptotic rates of cardiomyocytes in this pathological process and thus may have a protective effect on cardiomyocytes.