Preconditioning with mitochondrial ATP-sensitive potassium channel opener, diazoxide, protects the myocardial mitochondial functions after ischemic injury in rats

黄河; 肖颖彬; 杨天德; 李洪; 李永旺

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Preconditioning with mitochondrial ATP-sensitive potassium channel opener, diazoxide, protects the myocardial mitochondial functions after ischemic injury in rats

更新时间：2026-01-09

- Preconditioning with mitochondrial ATP-sensitive potassium channel opener, diazoxide, protects the myocardial mitochondial functions after ischemic injury in rats
- Journal of Army Medical University Vol. 30, Issue 9, Pages: 807-809(2008)
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  CLC： R364.12;R654.202;R972
- Published：2008
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黄河,肖颖彬,杨天德,李洪,李永旺.二氮嗪预处理对大鼠缺血性损伤心肌线粒体功能的保护作用[J].陆军军医大学学报(原第三军医大学学报),2008,30(09):807-809.

　HUANG He,XIAO Ying-bin,YANG Tian-de,LI Hong-,LI Yong-wang.Preconditioning with mitochondrial ATP-sensitive potassium channel opener, diazoxide, protects the myocardial mitochondial functions after ischemic injury in rats[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(09):807-809.
黄河,肖颖彬,杨天德,李洪,李永旺.二氮嗪预处理对大鼠缺血性损伤心肌线粒体功能的保护作用[J].陆军军医大学学报(原第三军医大学学报),2008,30(09):807-809. DOI：

　HUANG He,XIAO Ying-bin,YANG Tian-de,LI Hong-,LI Yong-wang.Preconditioning with mitochondrial ATP-sensitive potassium channel opener, diazoxide, protects the myocardial mitochondial functions after ischemic injury in rats[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(09):807-809. DOI：

摘要

目的探讨线粒体ATP敏感性钾通道开放剂二氮嗪预处理对大鼠心肌细胞线粒体功能保护作用。方法采用大鼠异丙肾上腺素心肌损伤模型，30只大鼠分成对照组、异丙肾上腺素（ISO）损伤组、二氮嗪（DZ）预处理组；以氧电极法测线粒体呼吸

罗丹明123 为荧光探针测定线粒体膜电位，采用定磷法检测Na

-ATP酶和Ca

-ATP酶活性。比较各组心肌细胞线粒体Ⅲ态呼吸速率、线粒体Ⅳ态呼吸速率、线粒体呼吸控制率和线粒体膜电位以及线粒体ATP酶的活性。结果 ISO组线粒体Ⅲ态呼吸速率呼吸控制率、线粒体膜电位以及Na

-ATP酶和Ca

-ATP酶活性与对照组比较显著下降(P0.01)；DZ预处理组Ⅲ态呼吸速率、呼吸控制率和线粒体膜电位(P0.05)以及Na

-ATP酶和Ca

-ATP酶活性较对照组低(P0.01)，但与ISO 组比较明显恢复。各组对Ⅳ态呼吸速率没有明显影响。结论线粒体ATP敏感性钾通道开放剂二氮嗪能增强心肌细胞线粒体酶活性，产生预处理心肌细胞线粒体保护效应。

Abstract

Objective To investigate the effect of preconditioning with mitochondrial ATP-sensitive potassium channel opener on the mitochondrial functions. Methods Thirty SD rats were used. Isoproterenol was used to induce myocardial ischemic injury in 20 rats

ten of which were pretreated with diazoxide. Rhodamine123 (Rh123) was used as fluorescent prober to measure mitochondrial membrane potential. The activities of mitochondrial Na

-ATPase and Ca

-ATPase were detected. The mitochondrial respiratory parameters were recorded with a Clark electrode. The effect of diazoxide on mitochondrial membrane potential and mitochondrial respiration was investigated. Results Compared with the controls

the levels of state 3 (ST3)

respiratory control rate (RCR)

mitochondrial membrane potential content and the activities of mitochondrial ATPase were decreased in the rats that received isoproterenol

while diazoxide pretreatment alleviated the changes of ST3

RCR

mitochondrial membrane potential and the activities of mitochondrial ATPase. Conclusion Preconditioning with diazoxide enhances the activities of mitochondrial ATPase and protects the myocardial mitochondrial function after isoproterenol induced myocardial ischemic injury.

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