【摘要】 目的研究雷米普利对大鼠心肌缺血再灌注损伤的影响,并初步探讨其作用机制。方法大鼠在体结扎冠状动脉前降支30 min后,松扎再灌注120 min制备心肌缺血再灌注损伤模型,计算心肌梗死范围(MIS),测定血清天门冬氨酸氨基转换酶(AST)、磷酸肌酸激酶(CK)、乳酸脱氢酶(LDH)、超氧物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)、一氧化氮(NO)含量,血浆内皮素(ET)、血管紧张素Ⅱ(AngⅡ)、前列环素(PGI2)及血栓素A2(TXA2)水平。结果雷米普利对心肌缺血30 min再灌注损伤120 min大鼠,可明显缩小MIS,降低血清AST、CK、LDH活性及MDA含量,提高NO含量及SOD、GSH-Px活性,能使血浆ET、AngⅡ及TXA2水平明显下降,PGI2水平及PGI2/TXA2比值明显增高。结论雷米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,减少内源性血管活性物质ET及AngⅡ释放,纠正PGI2/TXA2失衡等机制有关。更多还原

【Abstract】 Objective To investigate effect of Ramipril on myocardial ischemia-reperfusion injury in rats and its mechanism.Methods The myocardial ischemia-reperfusion model was induced by left anterior descending coronary occulusion in 30 min and reperfusion in 120 min in rats.The changes of myocardial infarct size(MIS),serum aspartate aminotransferase(AST),creatine phosphokinase(CK),lactate dehydrogenase(LDH),superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px) activities,malondialdehyde(MDA) and nitric oxide(NO) contents,and plasma endothelin(ET),angiotensinⅡ(AngⅡ),prostacycline(PGI2),thromboxane A2(TXA2) levels were determined.Results In rats treated by Ramipril,the MIS was significantly reduced,the serum AST,CK and LDH activities and MDA content were declined,but NO content,SOD and GSH-Px activities were increased markedly.In addition,the plasma ET,AngⅡ and TXA2 levels declined,while plasma PGI2 level and the ratio of PGI2/TXA2 was increased signficatly.Conclusion Ramipril is of protective effect on myocardial ischemia-reperfusion injury in rats by improving free radicals and myocardial metabolism,decreasing plasma ET,AngⅡ and TXA2 levels and increasing plasma PGI2 level and the ratio of PGI2/TXA2 etc.更多还原