优降糖对KATP通道介导缺血预适应心肌再灌注损伤的影响

目的 :探讨优降糖在完整大鼠心脏模型中 ,对 ATP敏感钾通道 (KATP)介导心肌缺血预适应作用的影响。方法 :将 4 4只大鼠随机分为 4组 :心肌缺血预适应组 (IPC组 )、优降糖组 (GL I组 )、优降糖 IPC组 (G P组 )和对照组 (C组 )。心肌缺血预适应由 3次 10分钟缺血和 10分钟再灌注组成。所有大鼠均接受 30分钟缺血和 6 0分钟再灌注。梗死范围由饱和曲利本蓝和红四氮唑蓝染色判定 ,并以坏死区占缺血区的百分比表示。 导联记录心脏室性心律失常。结果 :IPC能显著缩小缺血再灌注后的心肌梗死范围 ,且这种作用能被 KATP通道阻滞剂优降糖完全取消。 IPC可减少缺血再灌注所致的室性心律失常的发生 ,但这种保护作用不能被优降糖所阻断。结论 :优降糖对 KATP介导 IPC的心肌保护作用有影响。

Influence of glibenclamide on ATP-sensitive potassium channels in the cardiac ischemic preconditioning against myocardial ischemia-reperfusion injury

Objective:To study influence of glibenclamide on ATPsensitive potassium channels (K ATP ) in the effect on cardiac ischemic preconditioning (IP) against myocardial ischemiareperfusion injury. Methods: Fortyfour rats were divided into preconditioning group(IPC group),glibenclamide group(GLI group),glibenclamidepreconditioning group(GP group) and control group(C group). The preconditioning protocol consisted of 3 cycles of 10 minutes local ischemia and 3 cycles of 10 minutes reperfusion.The rats were subjected to 30 minutes of local ischemia followed by 60 minutes of reperfusion.The infarct size was measured by nitroblue tetrazolium and red tetrazolium staining.Results:IPC could result in marked reduction of infarct size,which was completely abolished by glibenclamide.IPC could also reduce the occurrence of ventricular arrhythmias induced by ischemiareperfusion,which failed to be blocked by glibenclamide.Conclusions:Glibenclamide can influence K ATP in cardiac protection of the intact rat IPC heart.