狗心肌缺血可逆与不可逆性损伤的超微结构  

Ultrastructure study on reversible and irreversible injure of myocardial ischemia of dog

作　　者：朱永宏[1] 杨书文[1] 李兰荪[1] 马淑坤[1] 史颖辉[2] 李学荣[2] 

机构地区：[1]西京医院心脏内科 [2]第四军医大学电镜室

出　　处：《第四军医大学学报》1993年第3期181-183,共3页Journal of the Fourth Military Medical University

摘　　要：作者在16只狗的晕厥心肌模型上进行了缺血及再灌注后不同时间点超微结构的动态观察,并同4只狗心肌梗塞的超微结构改变进行对比.结果表明晕厥心肌缺血15 min时,心肌细胞线粒体肿胀及空泡形成;糖原减少,T型管肿胀.再灌注5min时其损伤进一步加重,但膜性结构完整.之后逐渐恢复,至180min时大部分结构恢复接近正常.心肌缺血4h其线粒体肿胀崩解及球状致密物生成,肌膜出现微小缺损.说明心肌缺血可逆性与不可逆性损伤主要在于维持细胞膜结构的完整性.The ultrastructural changes of myocardial stunning and myocandial infarction were compared in 16 anesthetized open-chest dogs. Myocardial stunned by a 15 min transient ischemia was characterized by mitochondrial swelling, glycogen depletion and relaxation of sarcomere. Reperfusion for 5 min, the injure became severer than the phase of ischemia while the membranous structures still maintained intact. As the reperfusion went on, the damaged myocytes were gradually recovered. After 180 min reperfusion, the ultrastructural consequences of stunned myocardium were nearly reversed. Myocardial infaraction by 4 h ischemia was characterized by mitochondrial flocculent precipitates and damaged myolemma tine. The results showed that the intactness of membranous structure is important in reversible and irreversible injure of myocardial ischemia.

关 键 词：再灌注损伤 超微结构 心肌缺血 

分 类 号：R361.3[医药卫生—病理学]