ATP敏感性钾通道参与预缺血对麻醉家兔缺血心肌的保护

INVOLVEMENT OF ATP SENSITIVE POTASSIUM CHANNELS IN THE CARDIOPROTECTION PROVIDED BY ISCHEMIC PRECONDITIONING IN ANESTHETIZED RABBITS

在氨基甲酸乙酯麻醉家兔心肌缺血／再灌注模型上，观察了ＡＴＰ敏感性钾（ＫＡＴＰ）通道开放剂Ｃｒｏｍａｋｌｉｍ（Ｃｒｏ）和预缺血对血流动力学和心肌梗塞范围的影响，旨在阐明ＫＡＴＰ通道是否参与预缺血对缺血／再灌注心肌的保护机制。所得结果如下：①单纯缺血３０分钟－再灌注１８０分钟过程中，血流动力学各参数和心肌耗氧量均进行性降低，心肌梗塞范围为３２．３％。②静脉注射Ｃｒｏ后再进行缺血／再灌注时，心肌梗塞范围２３．３％，较单纯缺血／再灌注组明显减小（Ｐ＜０．０５），表明ＫＡＴＰ通道激活对缺血／再灌注心肌有保护作用。③预缺血后，心肌梗塞范围为２１．６％，与单纯缺血／再灌注组相比，有明显差异（Ｐ＜０．０１）；而ＫＡＴＰ通道特异性阻断剂格列苯脲则可阻断预缺血对缺血／再灌注心肌的保护效应，提示ＫＡＴＰ通道在预缺血心肌保护过程中起重要作用。以上结果表明，ＫＡＴＰ通道参与预缺血对心肌的保护机制。

The effects of ATP sensitive potassium channel (KATP channel) opener cromaklim (Cro) and ischemic preconditioning (IP) on the hemodynamics and myocardial infarct size were examined in the urethane-anesthetized rabbit model of myocardial ischemia reperfusion to define whether the KATP channel was involved in the cardioprotection provided by IP. The results obtained were as follows:①During the course of ischemia (30 min)-reperfusion (180 min), all hemodynamic parameters and myocardial oxygen consumption were decreased progressively, and the myocardial infarct size of the left ventricle was 32. 3±0. 8%. ②Prtreatment with Cro reduced the myocardial infarct size to 23. 3± 2. 2% (P<0. 05),indicating that the activation of KATP channels exerted a beneficial action on ischemiareperfused myocardium. ③IP signficantly reduced the infarct size to 21. 6 ± 1. 8% (P <0. 01),an effect which was abolished by glibenclamide, a potent KATP channel blocker. It was implied that the activation of KATP channel did play an important role in the cardioprotection provided by IP. From these results, it is suggested that the cardioprotection mechanism of IP was produced through the activation of KATP channels.