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用家犬制造实验性心肌缺血-再灌注动物模型,在心电图监测下,用间接和直接检测技术,在不同时间内分别检测汇常区,缺血-再灌注心肌的丙二醛(MDA)含量、谷胱甘肽过氧化物酶(GSH-px)及超氧化物歧化酶(SOD)的活性。结果,缺血-再灌注区心肌MDA高于正常区(P<0.05),GSH-px活性较正常区低,SOD活性在再灌注5min后持续上升,缺血30min后再灌注心肌标本直接低温测定电子自旋共振波谱显示氧自由基信号增强,提示心肌缺血后再灌注有氧自由基的异常增加,为心肌缺血一再灌注损伤的发生提供了依据。治疗组在再灌注前给子足量山莨菪碱,再灌后体内脂质过氧化损伤显著减轻,并呈量效关系。作者在临床抢救危重病患者28例取得满意效果,说明山莨菪碱能减少氧自由基的产生,防止膜的脂质过氧化损伤,提高细胞对缺血缺氧的耐受性。认为在再灌注的即时给予足量山莨菪碱配合其它抢救措施,可以预防或减轻再灌注损伤。
The experimental myocardial ischemia-reperfusion animal model was made in domestic dogs. MDA and MDA in ischemic-reperfused myocardium were detected by indirect and direct detection techniques under different electrocardiogram (ECG) Content, glutathione peroxidase (GSH-px) and superoxide dismutase (SOD) activity. The results showed that the myocardial MDA in ischemia-reperfusion area was higher than that in normal area (P <0.05), GSH-px activity was lower than that in normal area, and SOD activity increased continuously 5 minutes after reperfusion. Electron spin resonance spectroscopy showed that the signal of oxygen free radicals was enhanced, suggesting an abnormal increase of oxygen free radicals after myocardial ischemia and reperfusion, which provided a basis for the occurrence of myocardial ischemia / reperfusion injury. The treatment group before giving a sufficient amount of anisodamine before reperfusion, lipid peroxidation damage significantly reduced after reperfusion, and the dose-response relationship. The authors obtained satisfactory results in clinical rescue of 28 critically ill patients, indicating that anisodamine can reduce the production of oxygen free radicals, prevent membrane lipid peroxidation damage and improve the tolerance of cells to ischemia and hypoxia. It is considered that adequate administration of anisodamine together with other rescue measures during reperfusion can prevent or reduce reperfusion injury.