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ATP敏感性钾通道在预缺血对麻醉家兔缺血心肌保护中的作用

丁延峰, 何瑞荣

河北医科大学基础所生理室.河北,石家庄 050017

摘要

氨基甲酸乙酯和戊巴比妥钠两种不同麻醉动物模型在单纯缺血30 min-再灌注180 min过程中,血流动力学各参数和心肌耗氧量均进行性降低。K_(ATP)通道在氨基甲酸乙酯麻醉下参与IP的心肌保护机制。在戊巴比妥钠麻醉下,K_(ATP)通道并不参与IP的心肌保护过程。

关键词： 缺血-再灌注; 预缺血; ATP敏感性钾通道; 心肌梗塞范围

Role of K_(ATP) channels in the cardioprotection provided by ischemic preconditioning in anesthetized rabbits

Ding Yanfeng, He Ruirong

Department of Physiology, Institute of Basic Medicine, Hebei Medical University.Shijiazhuang 050017

Abstract

The effects of K_(ATP) channel opener cromaklim (Cro) and ischemic preconditioning (IP) on hemodynamics and myocardial infarct size were examined in both urethane and sodium pentobarbital anesthetized rabbit models of myocardial ischemia-reperfusion to determine whether the K_(ATP) channel was involved in the cardioprotection provided by IP. The results were as follows: (1) All hemodynamic parameters and myocardial oxygen consumption were decreased progressively during the course of ischemia (30 min)-reperfusion (180 min). (2) In the urethane anesthetized model, the myocardial infarct size of the left ventricle induced by ischemia-reperfusion was (32.3±0.8)%. pretreatment with Cro reduced the myocardial infarct size to (23.2±2.2)%, while IP signficantly reduced the infarct size to (21.6±1.8)%,which was abolished by a potent K_(ATP) channel blocker glibenclamide. (3) In the sodium pentobarbital anesthetized model, myocardial infarct size was (32.7±1.0)%. IP also reduced the myocardial infarct size to (19.7±1.5)%, which could not be blocked by cardioprotection of IP by glibenclamide. Cro failed to decrease inifarct size. Such results indicated that activation of K_(ATP) channels exerted a beneficial action on ischemia-reperfused myocardium only in the urethane anesthetized rabbit.

Key words: Ischemia-reperfusion;Ischemic preconditioning;ATP sensitive potassium channel;Myocardial infarct size

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引用本文：

丁延峰, 何瑞荣. ATP敏感性钾通道在预缺血对麻醉家兔缺血心肌保护中的作用[J]. 生理学报 1997; 49 (1): .

Ding Yanfeng, He Ruirong. Role of K_(ATP) channels in the cardioprotection provided by ischemic preconditioning in anesthetized rabbits. Acta Physiol Sin 1997; 49 (1): (in Chinese with English abstract).