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采用Ｌａｎｇｅｎｄｏｒｆ离体心脏灌注模型，对大鼠心肌缺氧—再给氧损伤中抗自由基酶ＳＯＤ和ＧＳＨ－Ｐｘ，过氧化产物ＭＤＡ、心肌酶ＣＰＫ和心肌细胞超微结构进行了观察、同时探讨了参麦注射液的保护作用机理。结果表明：（１）心肌缺氧灌注４０ｍｉｎ，富氧再灌５ｍｉｎ，与正常对照组比较，心肌细胞超微结构损伤严重，线粒体数目减少，大部分空泡变性，嵴消失，糖原颗粒减少，心肌收缩结构受到严重破坏。同时ＣＰＫ活性明显升高，ＳＯＤ及ＧＳＨ－Ｐｘ活性明显降低，ＭＤＡ含量明显升高（Ｐ＜０．０１）。（２）预先给不同剂量参麦注射液进行灌注，与模型组比较，心肌超微结构损伤明显减轻，线粒体数目较多，嵴密集，未见肿胀变形，糖原颗粒丰富，心肌收缩结构基本正常。ＣＰＫ活性明显降低，心肌ＳＯＤ及ＧＳＨ－Ｐｘ活性明显增高，心肌ＭＤＡ含量明显降低（Ｐ＜０．０１）。且参麦大剂量组疗效优于复方丹参液（Ｐ＜０．０５）。我们推测其保护作用机理可能是稳定心肌细胞膜，保护心肌线粒体，增加能量供应，提高抗自由基酶活性，从而减轻氧自由基对心肌的损害
The Langendorf perfusion model was used to observe the anti-free radical enzyme SOD and GSH-Px, the peroxidative product MDA, the myocardial enzyme CPK and the myocyte ultrastructure during myocardial anoxia-reoxygenation injury in rats The protective effect of Shenmai injection mechanism. The results showed that: (1) myocardial hypoxia perfusion 40min, oxygen enrichment and reperfusion 5min, compared with the normal control group, myocardial ultrastructure damage, reduce the number of mitochondria, most of the vacuolar degeneration, ridges disappear, glycogen particles decreased, Myocardial contractile structure is severely damaged. At the same time, the activity of CPK increased significantly, the activity of SOD and GSH-Px decreased significantly, MDA content increased significantly (P <0.01). (2) Compared with the model group, myocardial ultrastructure damage was preliminarily perfusion with different doses of Shenmai injection. There were more mitochondria, more crests, no swelling and deformation, abundant glycogen granules, and myocardial contractions were basically normal . CPK activity was significantly decreased, myocardial SOD and GSH-Px activity was significantly increased, myocardial MDA content was significantly lower (P <0.01). And Shenmai large dose group curative effect is better than compound Danshen liquid (P <0.05). We speculate that the mechanism of its protective effect may be to stabilize myocardial cell membrane, protect myocardial mitochondria, increase energy supply, improve anti-free radical enzyme activity, thereby reducing the damage of oxygen free radicals on the myocardium