局部肾素血管紧张素系统在心肌细胞氧反常中的作用  

The effect of local renin-angiotensin system(RAS) on cardial oxygen paradox

作　　者：朱甫祥[1] 马丽英[1] 王孝铭[1] 赵铁强[1] 李晓哲[1] 

机构地区：[1]哈尔滨医科大学病理生理教研室,哈尔滨150086

出　　处：《中国病理生理杂志》1997年第2期126-128,共3页Chinese Journal of Pathophysiology

摘　　要：利用成年大鼠分离的心肌细胞氧反常模型,用新一代钙荧光探针(Fluo-3)检测细胞内游离钙浓度。对比观察了血管紧张素Ⅱ及转换酶抑制剂(巯甲丙脯酸)对钙超载的影响。结果表明前者促成钙超载的形成,而后者可以防止钙超载。从而证明心肌细胞的肾素血管紧张素系统在氧反常时细胞钙超载中具有重要作用。To make 'oxygen paradox' model isolated rat myocytes was used. A new calcium fluoresence probe (Fluo-3) was used to detect the changes of free calcium in cardiac cells. The influence of angiotensin Ⅱ (AT Ⅱ) and angiotesin-Ⅰ converting enzyme inhibitor(ACEI captopril) on calcium overload in cardial cells was observed comparatively. The results showed that AT Ⅱ promoted calcium overload and ACE Ⅰ inhibited it, indicating cardial renin-angiotensin system(RAS) plays an important role in regulation of cellular calcium homeostasis during oxygen paradox and their possible mechanism was also discussed.

关 键 词：心肌缺血 血管紧张素 卡托普利 

分 类 号：R541.402[医药卫生—心血管疾病]