对K_(ATP)通道介导缺血预适应心肌再灌注损伤的研究

The influence of glybenzcyclamide on cardiac ischemic preconditioning against myocardial ischemia-reperfusion injury induced by ATP-sensitive potassium channels

目的探讨优降糖对KATP通道介导心肌缺血预适应作用的影响。方法将44只大鼠随机分为心肌缺血预适应组(IPC组)、优降糖组(GLI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10min缺血/10min再灌注组成。所有大鼠均接受30min缺血/60min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率表示。Ⅱ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。

Objective To study the effect of glybenzcyclamide （GLC） on cardiac ischemic preconditioning （IP） against myocardial iscbemia-reperfusion （IR） injury induced by ATP-sensitive potassium channels （KATP）. Methods 44 rats were randomly divided into IR preconditioning （IPC） group, GLC group, GLC-preconditioning （G-P） group and control groulx The preconditioning protocol consisted of 3 cycles of 10 min I/R The rats were subjected to 30min of local ischemia followed by 60 min of reperfusion. The infarct size was measured by nitroblue tetrazolium and red tetrazolium staining and signed by percentage of necrosis zone in ischemia zone. The cardiac ventricular arrhythmia was recorded by Ⅱ lead. Results IPC resulted in marked reduction in infarct size, which was completely abolished by glybenzcyclamide. IPC also reduced I/R induced ventricular arrhythmias,which couldn＇t be blocked by glybenzcyclamide. Conclusions Glybenzcyclamide could influence the protective role of KATP induced LPC myocardial preservation.