中文摘要：

目的：探讨乙醇后处理心肌保护作用是否与一氧化氮生成有关。方法：局部结扎冠状动脉左前降支30min,复灌120 min复制离体大鼠心肌缺血/复灌模型。心肌缺血末5 min,复灌初期10min给予乙醇50mmol/L,共灌流15 min进行乙醇后处理干预。实验随机分为五组,正常组,缺血/复灌组,乙醇后处理组,乙醇后处理＋L-NAME组和乙醇后处理＋苍术苷组。测定心室动力学指标和复灌期间冠脉流出液中乳酸脱氢酶（LDH）含量,TTC染色法测定心肌梗死面积,硝酸还原法测定心肌组织一氧化氮（NO）含量。RT-PCR检测左心室前壁心尖组织Bc-l2和BaxmRNA的表达。结果：与单纯缺血/复灌相比,乙醇后处理明显促进了左室发展压、左室做功的恢复,降低复灌期冠脉流出液中LDH的释放和心肌梗死面积,心肌组织NO释放减少,Bc-l 2/Bax mRNA比值增高。一氧化氮合酶抑制剂L-NAME和线粒体渗透性转换孔道开放剂苍术苷均抑制了乙醇后处理心室功能的恢复、LDH释放的减少和梗死面积的降低,心肌组织NO释放进一步减少,Bc-l 2/Bax mRNA比值降低。结论：乙醇后处理的心肌保护作用可能与减少NO的释放、抑制线粒体渗透性转换孔道的开放和抑制细胞凋亡的发生有关。

英文摘要：

Objective： To investigate whether the release of nitric oxide（NO） was involved in the cardioprotection of ethanol postconditioning in isolated rat hearts.Methods： Hearts isolated from male SD rats were subjected to 30 min of regional ischemia（occlusion of left anterior descending artery） followed by 120 min of reperfusion.Ethanol postconditioning was fulfilled through perfusion of 50 mmol/L ethanol for 15 min（at the end of cardiac ischemia for 5 min and at the beginning of reperfusion for 10 min）.The rats were divided into five groups： normal,ischemia and reperfusion,ethanol postconditioning,ethanol postconditioning＋L-nitro-arginine-methylester（L-NAME） and ethanol postconditioning＋atractyloside.The ventricular hemodynamic parameters and lactate dehydrogenase（LDH） release during reperfusion were measured.The infarct size was measured by TTC staining method and NO content was measured by nitric acid reductase method.The expressions of Bcl-2 and Bax mRNA were detected by RT-PCR analysis.Results： In contrast to ischemia and reperfusion,ethanol postconditioning improved left ventricular developed pressure,rate pressure product during reperfusion,reduced LDH release and infarct size.NO content was decreased.The ratio of Bcl-2/Bax was increased.Administration of nitric o-xide synthase inhibitor L-NAME or mitochondrial permeability transition pore opener atractyloside both attenuated the role of ethanol postconditioning,which inhibited the recovery of hemodynamic parameters,the decreases of LDH and infarct size.NO content was decreased furtherly.The ratio of Bcl-2/Bax was decreased.Conclusion： The cardioprotection of ethanol postconditioning may be associated with reducing nitric oxide release,inhibiting the opening of mitochondrial permeability transition pore and decreasing the happening of apoptosis.