钙通道激动剂Bay k 8644对重症失血性休克大鼠细动脉平滑肌细胞膜电位的作用  

Effect of Bay K 8644 on arteriole smooth muscle cell membrane potential in rats with severe hemorrhagic shock

作　　者：赵清[1] 赵克森[1] 

机构地区：[1]南方医科大学病理生理教研室,广东广州510515

出　　处：《南方医科大学学报》2006年第4期421-424,共4页Journal of Southern Medical University

基　　金：国家自然科学基金(30070735)~~

摘　　要：目的探讨平滑肌细胞外钙内流对正常膜电位和休克后期超极化膜电位状态的影响。方法制作失血性休克大鼠模型,分离血管平滑肌细胞(ASMCs),用DiBAC4(3)标记细胞膜电位,共聚焦显微镜观察Bay k 8644和TEA对正常对照组和休克组细胞膜电位的影响。结果 Bay k 8644使正常对照组的ASMCs膜电位超极化,而Bay k 8644对休克组 ASMCs膜电位的作用是去极化,但这种作用可被TEA逆转。结论在正常情况下外钙大量内流会激活BKCa使细胞膜电位超极化,而在休克后期外钙内流会直接导致ASMCs膜电位的去极化,对于休克后期低反应性的治疗有重要意义。Objective To investigate the effect of Ca^2＋ influx through L-type Ca^2＋ channels on normal and hyperpolarized membrane potential of arteriole smooth muscle cells （ASMCs） in rats. Methods The ASMCs isolated from normal rats and those with severe hemorrhagic shock were labeled with DiBAC4 （3） for membrane potential detection. Results Ca^2＋ influx caused hyperpolarization of the membrane potential in the normal ASMCs but depolarization in the cells from rats with hemorrhagic shock, and this effect could be inhibited by TEA. Conclusion Ca^2＋ -activated potassium channels activated by Ca^2＋ influx through L-type Ca^2＋ channels in normal ASMCs to cause hyperpolarization but leads directly to membrane potential depolarization in ASMCs from rats with severe hemorrhagic shock. This finding can be meaningful for treatment of vascular hyporeactivity in advanced stage of severe shock.

关 键 词：失血性休克 膜电位 L型钙通道 大电导钙激活钾通道 

分 类 号：R965[医药卫生—药理学]