摘要
本实验发现兔心缺血-再灌流损伤时,心律失常发生率、心肌钙含量以及脂质过氧化物MDA含量都明显增加,而肌质网Ca~(2+)-ATP酶活性明显降低,山莨菪碱有明显的保护作用。本文对其作用机制进行了初步探讨。
Anisodamine (A) had protective effects on ischemia-reperfusion injury. But its mechanism is still far from clear. The aim of this study was to investigate the changes of SR Ca~(2+)-ATPase activity during myocardial ischemia-reperfusion injury in rabbit and the effects of A. The rabbits were divided randomly into four groups, i. e., sham, ischemia (40-mine), ischemia (15-mins)-re-perfusion (25-mins) and A+ ischemia-reperfusion. A microsomal fraction enriched in SR vesicles was isolated from left ventricular myocardium in different groups. Decrease of SR Ca~(2+)-ATPase activity was found in the ischemic groups. Reperfusion after ischemia resulted in a further decrease of Ca~(2+)-ATPase activity. The Ca~(2+)contents, MDA production of cardiac homogenates and the incidence of arrhythmias in the ischemiareperfusion group increased significantly. A showed significant protective effects on bese changes induced by cardiac ischemia-rcperfusion injury in rabbils.
In vitro experiments showed that the depressant effect of oxygen free radicals induced by exogenous X/XOD system on normal cardiac SR Ca~(2+)-ATPase activity of rabbits was prevented by the addition of A (0.1mg/ml), as well as SOD (10μg/ml), and catalase (20μg/ml).
Results indicate that A may protect against peroxidation of membrane phospholipids induced by oxygen free radicals, stabilize SR membrane, protect SR Ca~(2+)-ATPase, reduce Ca~(2+) overload in the cytosole.
出处
《中国循环杂志》
CSCD
1991年第4期290-293,共4页
Chinese Circulation Journal
基金
国家科研“七五”攻关资助
关键词
山莨菪碱
心肌缺血
再灌注损伤
兔
Ischemia-reperfusion
SR Ca~(2+)-ATPase
Anisodamine
Oxygen fres radicals
Heart
