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实验分四组,采用非循环Langendorff灌注方法。结果表明缺氧心肌琥珀酸脱氢酶、超氧阴离子歧化酶和谷胱甘肽过氧化物酶活性降低,丙二醛升高;再给氧酶活性较缺氧显著下降,丙二醛明显增加;药物组酶活性较再给氧明显回升,丙二醛显著降低。超微结构显示有氧心肌正常;缺氧心肌细胞水肿,线粒体空泡变,核质凝聚,肌丝溶解;再给氧心肌损伤加重,挛缩带形成,镧涌入胞浆与线粒体内;药物组细胞损伤减轻,线粒体致密,嵴较完整,镧分布于膜外。实验结果提示心肌再给氧损伤与氧自由基毒性密切相关;地尔硫(艹卓)具有一定的防治作用,其机制值得深入探讨。
The experiment was divided into four groups, using non-cyclic Langendorff perfusion method. The results showed that the activity of succinate dehydrogenase, superoxide anion glutamase and glutathione peroxidase in hypoxic myocardium decreased and the malondialdehyde increased. The activity of reoxygenation enzyme decreased significantly compared with hypoxia, and malondialdehyde increased significantly ; The enzymatic activity of the drug group was significantly higher than that of the reoxygenation group and the malondialdehyde was significantly decreased. The ultrastructure showed normal myocardial oxygen; edema of hypoxic cardiomyocytes, vacuolization of mitochondria, condensation of nucleolus and myofilament; increased myocardial injury after injury, formation of contracture band, influx of lanthanum into cytoplasm and mitochondria; Mitigating cell injury, mitochondria dense, more complete ridges, lanthanum distribution in the membrane. Experimental results suggest that myocardial reoxygenation injury is closely related to oxygen free radical toxicity; diltiazem has some preventive and therapeutic effects, and its mechanism deserves further exploration.