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

ROLE OF K_(ATP) CHANNELS IN THE CARDIOPROTECTION PROVIDED BY ISCHEMIC PRECONDITIONING IN ANESTHETIZED RABBITS

在氨基甲酸乙酯和成巴比妥钠两种不同麻醉的家兔心肌缺血－再灌注（IR）模型上，观察了ATP敏感性钾通道（KATP通道）开放剂cromaklim（Cro）和预缺血（IP）对血流动力学和心肌梗塞范围的影响，旨在阐明KATP通道是否参与IP对IR心肌的保护机制。所得结果如下：（1）两种麻醉动物模型在单纯缺血30min-再灌注180min过程中，血流动力学各参数和心肌耗氧量均进行性降低。（2）在氨基甲酸乙酯麻醉的家兔，单纯IR所致的心肌梗塞范围为（32．3±0．8）％。静注Cro后再进行IR时，心肌梗塞范围为（3．3±2．2）％；IP后，心肌梗塞范围为（21．6±1．8）％；均与单纯IR组有明显差异。而KATP通道特异性阻断剂格列苯脲则可阻断IP对IR心肌的保护效应。以上结果显示KATP通道在氨基甲酸乙酯麻醉下参与IP的心肌保护机制。（3）在戊巴比妥钠麻醉的家兔，单纯IR时的心肌梗塞范围是（3．7±1．0）％。IP使IR的心肌梗塞范围减少至（19．7±1．5）％，格列苯脲未能取消IP对心肌的保护作用；Cro也未能减轻IR所致的心肌坏死。上述结果表明在戊巴比妥钠麻醉下，KATP通道并不参与IP的心肌保护过程。

The effects of KATP channel opener cromaklim (Cro) and ischemic preconditioning(IP) on hemodynamics and myocardial infarct size were examined in both urethaneand sodium pentobarbital anesthetized rabbit models of myocardial ischemia-reperfusionto determine whether the KATP channel was involved in the cardioprotection provided byIP. 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 infarctsize of the left ventricle induced by ischemia-reperfusion was (32. 3± 0. 8 ) %. Pretreatment with Cro reduced the myocardial infarct size to (23. 3±2. 2 ) %, while IPsignficantly reduced the infarct size to (21. 6± 1. 8) %, which was abolished by a potent KATP channel blocker glibenclamide. (3) In the sodium pentobarbital anesthetizedmodel,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 byglibenclamide. Cro failed to decrease infarct size. Such results indicated that activationof KATP channels exerted a beneficial action on ischemia-reperfused myocardium only inthe urethane anesthetized rabbit.