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作 者:韩红[1] 李麟仙[1] 王琼仙[1] 魏均娴[1] 陈业高[1]
机构地区:[1]昆明医学院病理生理教研室,昆明医学院植化研究室
出 处:《中国病理生理杂志》1994年第2期128-133,共6页Chinese Journal of Pathophysiology
摘 要:采用Langendorff离体心脏灌流方法,以停灌30分钟,再灌注20分钟制备大鼠心肌缺血再灌损伤模型。三七总皂甙(PNS30mg/L)和绞股兰总皂甙(GP,30mg/L和50mg/L)显著降低不可逆室颤发生率,50mg/L的GP显著抑制心肌LDH释放,PNS和GP显著提高缺血再灌心肌SOD活性,GP明显降低其MDA水平,PNS明显降低心肌钙含量。在结扎家兔冠状动脉左室支2小时,再灌注30分钟所造成的心肌缺血再灌损伤模型中,珠子参总皂甙PJS,250mg/kg)和PNS(200mg/kg)轻度改善缺血再灌后的左室功能,显著降低再灌后血浆LDH和CPK水平,明显减轻心肌钙聚积。以上结果表明:PJS,PNS和GP对心肌缺血再灌损伤具有保护作用,PJS和PNS的作用机理可能与拮抗钙有关,GP的作用机理可能与抗脂质过氧化有关。Myocardial injury of isolated perfused rat heart was induced by 30 min global ischemia and 20 min reperfusion. It was found that PNS(30 mg/L)and GP(30 mg/L or 50 mg/L lowered the irrevisible VF rate. GP ( 50 mg/L supressed the release of LDH from rat heart at reperfusion significantly.In addition, PNS alleviated the reper fused myocardial calcium accumulation markedly and GP reduced myocardial MDA con tent obviously. Both PNS and GP elevated the reperfused myocardial SOD activity. In an other model, myocardial injury was produced in rabbit by ligation of left ventricular coro nary artery for 2 br folloWed by 30 min reperfusion, It was found that PNS(200 mg/k8)and PJS(250 mg/kg )partially ameliorated left venticular functions and reducedplasmal LDH and CPK level very much at reperfusion. Calcium accumulation in the re perfused Myocardium was much lessened. These results suggested that PNS, PJS and GPpossess protective effects on myocardial damag caused by ischemia and reperfusion. It alsosuggested that the underlying protective mechanisms of PJS and PNS are related to theprevention of calcium overload, and that GP has an action of anti lipid peroxidation.
分 类 号:R259.422[医药卫生—中西医结合]
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