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作 者:陈义汉[1] 黄宗勤[1] 张伟[2] 杨毓麟[2]
机构地区:[1]南通医学院附属医院心内科 [2]南通医学院药理教研组
出 处:《江苏医药》1992年第5期234-236,共3页Jiangsu Medical Journal
摘 要:采用大鼠离体工作心脏,观察卡托普利(CAP)对心肌缺血再灌注损伤的保护作用。结果表明:CAP 减少心肌肌酸磷酸激酶(CPK)释放、减少心肌丙二醛(MDA)生成、降低心肌细胞内钙含量、减少再灌注诱发的室颤(VF)和室速(VT)的发生率,并对心肌超微结构具有保护作用。作者还把CAP 和超氧化物歧化酶(SOD)作了比较。提示CAP 具有自由基清除作用,对心肌缺血再灌注损伤具有保护作用。Protective effects of captopril on myocardial ischemia and reperfusioninjury were studied with isolated rat hearts.Catopril significantly decreased creatinekinase(CPK)release,reduced malondialdehyde(MDA)production and attenuated myoca-rdial Ca^(2+) accumulation,Furthermore it reduced incidences of reperfusion—induced ventr-icular fibrillation(VF),ventricular tachycardia(VT)and prevented myocardial ultrastr-uctural damage.We also compared captopril with SOD.The results suggest that captoprilpossesses scavenging action against oxygenderived free radicials.We conclude that captoprilhas protective effects on myocardial ischemia and reperfusion injury.
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