Objective It is to observe the protective effect of Shenmai Injection on myocardial ischemia reperfusion injury in rats.Methods 8 healthy rats were used as control group, the other 20 rats by ligation of left anterior descending coronary ar-tery for 30 min release buckles reperfusion 60 min to make the model of myocardial ischemia-reperfusion injury, and randomly divided into model group and Shenmai group.Three groups of rats were treated by tail intravenous injection with NS or Shen-mai Injection.before and after treatment for 1, 2 weeks, the levels of serum creatine kinase(CK), serum malondialdehyde (MDA), total superoxide dismutase (T-SOD), endothelin-1 (ET-1) and nitric oxide (NO) content were detected, and the myocardial ischemic area was measured in after 2 weeks of treatment.Results After the model of myocardial ischemia -reperfusion injury were established in model group, the levels of serum MDA, CK, ET-1 were markedly increased ( all P<0.05), and the T-SOD activity and NO content were markedly decreased (all P<0.05).After treated by Shenmai Injection in Shenmai group, the levels of serum MDA, CK, ET-1 were markedly decreased (all P<0.05), and the T-SOD activity and NO content were markedly increased (all P<0.05), the myocardial ischemic area were reduce significantly compared with model group (P<0.05).Conclusion Shenmai injection has protective effects on myocardial ischemia of rats, and its mechanism may be it can improve the free radical scavenging enzyme activity, promote production of NO to remove oxygen free radical, reduce lipid peroxidation, vascular endothelial dysfunction to improve reperfusion injury.%目的：观察参麦注射液对大鼠心肌缺血再灌注损伤的保护作用。方法选取8只健康大鼠为对照组，另16只大鼠采用结扎左侧冠状动脉前降支30 min后松解扎扣再灌注60 min以制作心肌缺血再灌注损伤模型，并随机分为模型组及参麦组。3组大鼠均经尾静脉分别注射生理盐水或参麦注射液，于给药前及给药后1周、2周分别测定血清肌酸激酶（ CK）、血清丙二醛（ MDA）、总超氧化物歧化酶（ T－SOD ）、内皮素－1（ ET－1）及一氧化氮（ NO）含量，并于治疗2周后测量心肌缺血面积。结果模型组大鼠造模后MDA、CK及ET－1含量均明显增高（P均＜0．05），T－SOD及NO含量明显下降（P均＜0．05）。在应用参麦注射液后，MDA、CK及ET－1含量均有不同程度的降低（P均＜0．05），T－SOD及NO含量均增高（P均＜0．05），且心肌缺血面积低于模型组（P＜0．05）。结论参麦注射液对大鼠缺血再灌注损伤有一定的防治作用，其作用机制可能是提高自由基清除酶活性，促进NO产生以清除氧自由基，减少脂质过氧化，改善再灌注损伤血管内皮功能紊乱。
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