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目的：从细胞保护的角度出发，观察米搞心乐滴丸（ＭＸＬＤＰ）对大鼠心肌缺血再灌注损伤的保护作用。方法：在结扎大鼠冠状动脉左前降支（ＬＡＤ）４５ｍｉｎ复灌后复制出的大鼠心肌缺血再灌注损伤模型上，研究ＭＸＬＤＰ对氧自由基的清除效能和血清一氧化氮（ＮＯ）含量。结果：ＭＸＬＤＰ（３０ｍｇ／ｋｇ和１２０ｍｇ／ｋｇ）能显著保护大鼠心肌组织超氧化物歧化酶（ＳＯＤ）活性，降低心肌组织中丙二醛（ＭＤＡ）含量和减少心肌细胞肌酸磷酸激酶（ＣＰＫ）的释放。能显著缩小梗塞面积，降低乳酸脱氢酶（ＬＤＨ）活性并能增加血清ＮＯ浓度，与生理盐水对照组比较差异显著（Ｐ＜０．０５，Ｐ＜０．０１）。结论：ＭＸＬＤＰ对大鼠心肌缺血再灌注损伤有保护作用，作用机理与抗氧化作用有关，也与防止ＮＯ释放减少有关。
OBJECTIVE: To observe the protective effect of Michangxindeli pill (MXLDP) on myocardial ischemia-reperfusion injury in rats from the perspective of cell protection. METHODS: The scavenging efficiency of oxygen free radicals and serum nitric oxide (NO) content were studied in a rat model of myocardial ischemia-reperfusion injury after ligation of the left anterior descending coronary artery (LAD) for 45 min. . RESULTS: MXLDP (30mg/kg and 120mg/kg) could significantly protect the activity of superoxide dismutase (SOD) in myocardium, decrease the content of malondialdehyde (MDA) in myocardium and reduce the myocardial cell creatine phosphokinase (CPK). ) The release. It can significantly reduce the infarct size, reduce the activity of lactate dehydrogenase (LDH) and increase the serum NO concentration, and there is a significant difference compared with the saline control group (P<0.05, P<0.01). Conclusion: MXLDP has a protective effect on myocardial ischemia-reperfusion injury in rats. Its mechanism of action is related to anti-oxidation and it is also related to prevention of NO release.