缺血预适应KATP通道的实验研究

目的探讨KATP通道在缺血预适应（ischemic preconditioning，IP）中所起的作用。方法建立在体犬鼠缺血再灌（ischemia／reperfusion，IR）模型，将60只犬鼠随机分为5组：缺血再灌（IR）组，缺血预适应（IP）组，尼可地尔（NIC）组，格列苯脲（GLI）组，5-HD组。分别测定各组的心肌梗死范围，血清CK，LDH浓度，监测各组心电图，应用透射电镜观察其超微结构的变化。结果相对与IR组，IP组明显的减少了心律失常分值和室颤发生率（P〈0．05），而5-HD组，NIC组则有加重心律失常发生的趋势；相对IR组，NIC组可部分模拟IP作用，而5-HD组则完全取消了IP的抗心肌缺血的保护作用。结论KATP通道可能是IP发生的效应器；线粒体KATP通道特异性阻滞剂能阻断KATP通道的抗心肌缺血的作用，推测至少在缺血阶段，线粒体KATP通道在IP中发挥了主要的作用。

Investigation of KATp channel on ischemic preconditioning

Objective] To investigate the effect of KATP channel on ischemic preconditioning. Methods] The snare for occlusion and reperfusion had been put into the anterior descending coronary artery in 60 rats which were divided into 5 groups: ischemic/reperfusion (IR) group, ischemic preconditioning (IP) group, nicorandil (NIC) group, glibenclamide (GLI) group, 5-HD group. The activity of creatine kinase (CK) and lactate dehydrogenase (LDH) in plasma and the infarct size were measured. The episode of arrhythmias was monitored. The ultrastructural changes of the myocardium were observed under electron microscope. Results] Compared with IR group, IP groups decreased significantly the incidence of ventricular fibrillation and arrhythmia scores (P<0.05), however, the arrhythmia of 5-HD group was aggravated. Compared with IR group, NIC group could mimic part of cardioprotective effect of IP group. The cardioprotective effect was completely disappeared in 5-HD group. Conclusions] It is suspected that KATP channel is the effector of ischemic preconditioning. The effect of anti-ischemic cardioprotection is blocked by mitokATP-selective antagonist-glibenclamide. It is suspected that mitochondrial KATP channel plays a primary role in ischemic period of ischemic preconditioning.