一氧化氮在乳鼠心肌细胞缺氧—复氧预处理延迟保护效应中的作用

探讨缺氧—复氧损伤对乳鼠心肌细胞一氧化氮释放和一氧化氮合酶活性的影响以及一氧化氮在心肌细胞延迟缺氧预处理中的作用。在培养乳鼠心肌细胞缺氧预处理的模型上，测定缺氧—复氧损伤对乳鼠心肌细胞一氧化氮释放和一氧化氮合酶活性，观察延迟缺氧预处理以及N-硝基-L-精氨酸、L广精氨酸、硝普钠对心肌细胞延迟缺氧预处理的影响。结果发现，缺氧—复氧后乳鼠心肌细胞一氧化氮释放增加，一氧化氮合酶活性升高。延迟缺氧预处理可以减少缺氧一复氧对心肌细胞的损伤。非选择性一氧化氮合酶抑制剂N-硝基-L-广精氨酸可以阻断延迟缺氧预处理的心肌保护作用，L广精氨酸不能模拟延迟缺氧预处理，硝普钠可以模拟延迟缺氧预处理。结果提示，一氧化氮可以诱导心肌细胞的延迟缺氧预处理。

Effects of Nitric Oxide on Delayed Protection of Cardiomyocyte Hypoxia/Reoxygenation Pretreatment

Aim To investigate the influence of nitric oxide (NO), nitric oxide synthase (NOS) on cardiomyocyte hypoxia/reoxygenation and effects of NO on cardiomyocytes delayed protection (DP). Methods The content of NO, NOS were measured in the models of hypoxia/reoxygenation (H/R) of cultured neonatal rat cardiomyocytes. The cell viability, lactate dehydrogenase (LDH) release, and the content of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured in the models of DP of cultured neonatal rat cardiomyocytes, with pretreatment of L-NA, L-arginine, sodium nitroprusside (SNP). Results NO and NOS increased significantly after transient hypoxia/reoxygenation. Hypoxic DP attenuated cardiomyocyte injure induced by H/R. Pretreatment with non-selective NOS inhibitor L-NA abolished the protectiive effect of hypoxia DP, L-arginine can not mimicked DP, but SNP may mimicked DP. Conclusion NO may be involved in the protection mechanism of DP.