mKATP对七氟醚后处理大鼠心肌细胞超微结构的影响

目的观察线粒体依赖ATP敏感钾通道（mKATP）的开放对七氟醚后处理大鼠心肌的保护作用。方法健康成年雄性SD大鼠32只，体重220～280g，将其随机分为4组（n=8）：假手术组（S组）、缺血再灌注组（IR组）、七氟醚后处理组（S-Post组）、七氟醚后处理＋拈抗剂组（S-Post＋5一HD组）。采用结扎冠状动脉左前降支法制备大鼠心肌缺血再灌注模型。观察各组心肌细胞超微结构变化，并计算梗死面积。结果与S组心肌梗死面积（7±1．7）％相比，其余各组显著增高（P〈0.05）；与IR组心肌梗死面积（50±2．8）％相比，S-Post组心肌梗死面积（36±2．2）％显著降低（P〈0．05），心肌细胞损伤轻；S-Post＋5-HD组心肌梗死面积（48±2．5）％与IR组差异无统计学意义（P〉0．05）。结论七氟醚后处理对大鼠缺血再灌注心肌具有保护作用，而这种保护作用与mKATP通道的开放有关。

The effect of mitochondrial KATP-channels on myocardial ultrastructure in the rat of sevoflurane postconditioning

Objective To investigate effects of sevoflurane on myocardial ischemia-reperfusion in rat in vivo and the role of mKATP channel. Methods Thirty-two male SD rats of clean grade weighing 220-280 g were randomly divided into 4 groups, and every group was 8 rats. Sham operation group （group S）, Ischemia and reperfusion group （group IR）, sevoflurane postconditioning group（group S-Post）and inhibitor group（group S-Post＋5-HD）. The model of the my- ocardial ischemia reperfusion was prepared by ligating the left anterior descending coronary artery. The myocardial ul- trastructures were investigated by electron microscope and detected myocardial infarct area. Results Compared with group S, infarct size in other three groups were significantly higher （P 〈 0.05） ;Compared with group IR,infarct size in group S-Post was significantly lower and the myocardial injury was relieved （P 〈 0.05） ;There was no significant difference between group S-Post＋5-HD and group IR （P 〉 0.05）. Conclusion Sevoflurane postconditioning can pro- tect myocardium IR injury in rats and mKATP channel is involved.