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本实验分别用大鼠在体、离体心脏和培养心肌细胞观察了卡托普利(甲巯丙脯酸)抗心肌缺血再灌注损伤与抗脂质过氧化作用。离体心脏缺氧缺糖45 min后再给氧30 min以及在体心脏缺血3 h后再灌注1h,心肌超氧化物歧化酶(SOD)活性明显下降而丙二醛(MDA)含量显著升高。卡托普利能显著保护再灌注(或再给氧)时心肌SOD活性和降低MDA含量。培养心肌细胞缺氧缺糖6 h,细胞MDA含量和乳酸脱氢酶(LDH)释放显著增加。卡托普利显著降低MDA含量和LDH释放。该作用能被吲哚美辛所取消。IIoprost显示有卡托普利相似的保护作用。结果表明卡托普利的保护作用与抗氧自由基和抗脂质过氧化有关。其机理主要通过促进心肌前列环素释放而发挥作用。
In this experiment, we observed the anti-myocardial ischemia-reperfusion injury and anti-lipid peroxidation of captopril (Captopril) in rat, isolated heart and cultured cardiomyocytes respectively. Myocardial superoxide dismutase (SOD) activity was significantly decreased and malondialdehyde (MDA) content was significantly increased after oxygen was deprived of glucose for 45 min in the isolated heart for 30 min and then in the ischemic myocardium 3 h after reperfusion for 1 h high. Captopril can significantly protect myocardium from reperfusion (or reoxygenation) SOD activity and reduce MDA content. After cultured for 6 h, the content of MDA and the release of lactate dehydrogenase (LDH) in cardiomyocytes increased significantly. Captopril significantly reduced MDA content and LDH release. This effect can be canceled by indomethacin. IIoprost shows a similar protective effect of captopril. The results show that the protective effect of captopril and antioxidant free radicals and anti-lipid peroxidation. Its mechanism mainly through the promotion of myocardial prostacyclin release play a role.