摘要
目的本研究旨在确定在完整大鼠模型中，心肌缺血预适应是否具有心肌保护作用，且这种保护作用是否由KATP通道介导。方法将48只大鼠随机分为4组：对照组、IPC组、优降糖十IPC组和优降糖组。所有动物均接受30min缺血／2h再灌注。预适应方案由3次5min缺血／5min再灌注组成。梗塞大小由硝基四唑氮蓝染色判定，并以坏死区占危险区的百分率表示。结果IPC几乎完全抑制了缺血/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KATP通道阻滞剂优降糖所阻断。IPC也能显著缩小缺血/再灌注后的心肌梗塞范围，且这种作用能被优降糖完全取消。结论IPC的心肌保护作用是由KATP介导的。
Objective To investigate whether the myocardial ischemic preconditioning (IPC) has cardioprotective effect and the effectis mediated by ATP-sensitive potassium channels (KATP). Method Forty-eighty rats were subjected to 30 min of local ischemiafollowed by 2 h of reperfusion. The preconditioning protocol consisted of 3 cycles of 5 min of local ischemia and 3 cycles of 5 minof reperfusion. The infarct size was measured by nitroblue tetrazolium staining. Result IPC almost completely abolished ischemia-and reperfusion-induced ventricular arrhythmias, which failed to be blocked by glibenclamide. IPC also resulted in marked reductionin infarct size, which was completely abolished by glibenclamide. Conclusion KATP, is involved in IPC-induced cardioprotection inthe intact rat hean.
出处
《第一军医大学学报》
CSCD
1999年第4期318-320,共3页
Journal of First Military Medical University
关键词
缺血预适应
心肌缺血
ATP敏感
钾通道
ischemic preconditioning
myocardial protection
ATP-sensitive potassium channels
Ischemia-reperfusion injury
