雷米普利对大鼠急性心肌梗死的保护作用及其机制  

Effect of Ramipril on experimental myocardial infarction in rats and its mechanism

作　　者：陈满秋[1] 陈冬梅[1] 王玉梅[1] 李迎今[1] 李洋[1] 赵学忠[1] 

机构地区：[1]吉林大学第一医院急救医学科,吉林长春130021

出　　处：《中国实验诊断学》2007年第10期1321-1324,共4页Chinese Journal of Laboratory Diagnosis

摘　　要：目的探讨雷米普利对大鼠实验性心肌梗死的保护作用及其机制。方法通过大鼠结扎左冠状动脉前降支(LAD)产生急性心肌梗死模型,观察雷米普利对实验性心肌梗死大鼠心肌梗死面积(MIS)及血清心肌酶学的影响,并从自由基及体内血管活性因子等变化分析其可能的作用机制。结果雷米普利可使实验性心肌梗死大鼠的MIS明显缩小,血清肌酸磷酸激酶(CK)、乳酸脱氢酶(LDH)、天门冬氨酸氨基转换酶(AST)活性及丙二醛(MDA)含量明显降低,血清超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性明显增加,亦可使血浆内皮素(ET)、血管紧张素Ⅱ(AngⅡ)及血栓素A2(TXA2)水平明显下降,前列环素(PGI2)水平及PGI2/TXA2比值明显增高。结论雷米普利对大鼠急性心肌梗死具有明显保护作用,可能与其增强抗氧化酶活性,减少自由基及血管活性因子对心肌的损伤,纠正心肌缺血时PGI2/TXA2失衡等机制有关。Objective To approach the protective effect of Ramipril on experimental myocardial infarction in mrs and its mecha- nism.Methods The effects of Ramipril on myocardial infarct size （MIS） and serum myocardial enzymology were observed and possible mechanism of action was analyzed with the changes of free radicaI and vascular active factors in vivo. Results In rats treated by Ramipril, the M：IS was significantly reduced, the activities of serum creatine phosphokinase （CK）, lactate dehydrogenase （LDH） and aspartate aminotransferase （AST）, the content of serum malondialdehyde （MDA） and the level of plasma endothelin （ET）, angiotensin Ⅱ （AngⅡ） and thromhaxane A2 （TXA2） were declined, while the activities of serum superoxide dismutaac （SOD） and glutathione peroxidase （GSH-Px）,the level of plasma prostacycline （PGI2） and the ratio of PGI2/TXA2 were increased markedly. Conduslon Ramipril have protective effect on acute myocardial infarction in rats by increasing anti-oxidase activity, reducing the damage of free radicals and vasoactive factors on myocardium, and correcting disequilibrium of PGI2/TXA2 in myocardial ischemia etc.

关 键 词：雷米普利 心肌梗死面积 心肌酶学 自由基 血管活性因子 大鼠 

分 类 号：R542.22[医药卫生—心血管疾病]