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目的:观察福辛普利对大鼠心肌缺血再灌注损伤的保护作用。方法:采用在体大鼠结扎冠状动脉前降支30min后,松扎再灌注24h造成心肌缺血再灌注模型,测定血清天冬酸氨基转移酶(AST)、乳酸脱氢酶(LDH)、心肌型肌酸激酶同功酶(CKMB)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSHPx)活性及丙二醛(MDA),通过光镜和电镜观察心肌组织形态学。结果:福辛普利对心肌缺血30min再灌注损伤24h大鼠,可明显降低血清AST、LDH及CKMB活性(P<0.05),提高SOD及GSHPx活性,降低MDA(P<0.05或P<0.01),并能明显减轻心肌组织水肿以及超微结构的损伤。结论:福辛普利对大鼠心肌缺血再灌注损伤具有明显保护作用,可能与其增强抗氧化酶活性,减少自由基对心肌的氧化损伤有关。
Objective: To observe the protective effect of fosinopril on myocardial ischemia-reperfusion injury in rats. Methods: Myocardial ischemia-reperfusion model was induced by ligating the anterior descending coronary artery in rats for 30 minutes after reperfusion, and the serum levels of aspartate aminotransferase (AST), lactate dehydrogenase (LDH), myocardium (CKMB), superoxide dismutase (SOD), glutathione peroxidase (GSHPx) activity and malondialdehyde (MDA) were detected by light microscope and electron microscope. . Results: Fosinopril could decrease the activities of serum AST, LDH and CKMB (P <0.05), increase the activities of SOD and GSHPx and decrease the levels of MDA (P <0.05 or P <0.01) ), And can significantly reduce myocardial tissue edema and ultrastructure damage. CONCLUSION: Fosinopril has a significant protective effect on myocardial ischemia-reperfusion injury in rats, which may be related to the enhancement of antioxidant enzyme activity and the reduction of oxidative damage induced by free radicals.