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目的 探讨吗啡预处理的晚期心肌保护作用以及诱导型一氧化氮合酶 (iNOS)在此过程中的作用。方法 建立在体小鼠冠状动脉阻断的心肌缺血再灌注模型。吗啡预处理 2 4h后 ,小鼠心肌缺血 4 5min ,再灌注 12 0min。用氯化三苯四唑 ( 2 ,3,5 triphenyltetrazoliumchloride ,TTC)染色确定梗死心肌范围。心肌梗死范围以梗死心肌 (IS)占缺血区心肌 (AAR)的重量百分比表示。并观察选择性iNOS抑制剂 (S methylthioureasulfate ,SMT)和iNOS基因敲除对吗啡预处理心肌保护作用的影响。结果 缺血再灌注后野生对照组IS/AAR为 4 3%± 5 % ,2 4h前给予吗啡可以使IS/AAR显著降低至 2 2 %± 4 % (P <0 0 5 )。吗啡预处理后再给予SMT可以取消吗啡的心肌保护作用。吗啡预处理对iNOS基因敲除小鼠完全没有心肌保护作用。结论 吗啡预处理具有晚期心肌保护作用。iNOS介导了吗啡预处理的晚期心肌保护作用
Objective To investigate the effect of morphine preconditioning on myocardial protection in the late stage and the role of inducible nitric oxide synthase (iNOS) in this process. Methods The model of myocardial ischemia-reperfusion induced by coronary artery occlusion in mice was established. Morphine pretreatment 2 4h, the mouse myocardial ischemia 4 5min, reperfusion 12 0min. Myocardial infarct size was determined by staining with triphenyltetrazolium chloride (TTC). Myocardial infarct size is expressed as the weight percentage of infarcted myocardium (IS) to ischemic myocardium (AAR). The effects of selective iNOS inhibitor (SMT) and iNOS knockout on the myocardial protection of morphine preconditioning were observed. RESULTS: IS / AAR was 43.3% ± 5% after ischemia-reperfusion, and morphine was significantly reduced to 22% ± 4% (P <0.05) at 24 hours. After morphine pretreatment and then given SMT can cancel the myocardial protection of morphine. Morphine preconditioning has no cardioprotective effect on iNOS knockout mice at all. Conclusion Morphine preconditioning has late myocardial protection. iNOS mediates late cardioprotection of morphine preconditioning