二氮嗪对大鼠心肌线粒体膜电位及呼吸功能的影响  

Effects of diazoxide on membrane potential and respiration function of rat cardiac mitochondria

作　　者：曾源[1] 龙超良[1] 慕邵峰[1] 李艳芳[2] 汪海[1] 

机构地区：[1]军事医学科学院毒物药物研究所,北京100850 [2]解放军总医院南楼心肾科,北京100853

出　　处：《中国临床药理学与治疗学》2004年第5期490-493,共4页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：军队医药卫生"十五"重点课题 (№ 0 1Z0 2 5 )

摘　　要：目的 :研究二氮嗪对大鼠心肌线粒体功能的影响 ,以探讨其心肌保护作用的可能机理。方法 :以罗丹明 12 3为荧光探针测定线粒体膜电位 ,氧电极法测线粒体呼吸 ,观察二氮嗪对正常大鼠心肌线粒体跨膜电位及呼吸的影响。结果 :5 0 μmol·L-1的二氮嗪可引起线粒体膜电位去极化 ,此影响可被钾通道阻滞剂消除 ;二氮嗪 10 0 μmol·L-1可降低大鼠心肌线粒体琥珀酸链的R3、R4速率 ,但不影响呼吸控制率。结论 :二氮嗪可调节大鼠心肌线粒体功能 ,这与其抗心肌缺血保护作用有关。AIM: To study the effects of selective mitoK_ ATP opener diazoxide on the isolated mitochondria from rat hearts and to discuss its cardioprotective mechanism. METHODS: Using Rhodamine123 (Rh123) as fluorescent prober to measure mitochondrial membrane potential and to record mitochondrial respiratory parameters with a Clark electrode,the effect of diazoxide on mitochondrial membrane potential and mitochondrial respiration were investigated. RESULTS: 50 μmol·L -1 diazoxide could induce mitochondrial membrane depolarization and this effect was abolished by application of a K_ ATP channel blocker. It could decrease R3 and R4 while oxidizing FAD-dependent substrates (succinate) but did not affect respiratory control ratio (RCR). CONCLUSION: Modulation by diazoxide on functions of rat cardiac mitochondria is associated with its anti-ischemic efficacy.

关 键 词：二氮嗪 线粒体 氧电极法 线粒体膜电位 

分 类 号：R965.1[医药卫生—药理学]