Hypoxia-induced apoptosis of cardiomyocyte and the protection of nitric oxide

Aim To study the role of hypoxiainduced apoptosis in neonatal rat cardiomyocyte and the protection effect of nitric oxide(NO). Methods Neonatal rat cardiomyocytes were cultured in an incubator of 950 mL/L N 2 and 50 mL/L CO 2 for 16, 32 and 48 h to create cell models of hypoxia injury and detect apoptosis. And NO donor SNAP at 100 μ mol/L was added to the models. Apoptosis was detected in the hypoxia cells without or with No treatment. Results After hypoxia of 16, 32 and 48 h,the apoptosis rates of cardiomyocytes were 29% ± 05% , 62% ± 08% and 266% ± 30% , respectively. Whereas the apoptosis rates of cells treated with SNAP were 02% ± 03% , 34% ± 04% and 118% ± 12% , respectively. Conclusion Apoptosis is the main form of hypoxia injury in cardiomyocytes; NO protect cardiomyocytes from apoptosis induced by hypoxia.