K_(ATP)通道在缺血预调中作用机制的实验研究  

Experimental study on the mechanism of K_(ATP) channel in ischemic preconditioning

作　　者：周睿[1] 朱洪生[1] 

机构地区：[1]上海第二医科大学附属仁济医院胸外科,上海胸科医院心血管外科200001

出　　处：《上海医学》2002年第10期619-622,共4页Shanghai Medical Journal

摘　　要：目的　研究缺血预调和腺苷的心肌保护作用是否与ATP敏感的钾离子通道 (KATP通道 )开放有关。方法　用缓冲液灌注 36只离体兔心脏 ,保护含钾液停跳 ,常温缺血 30min ,复灌 6 0min ,并随机分成 6组。第 1组 :对照组 ;第 2组 :缺血预调组 ;第 3组 :腺苷组 (2 0 μmol/L) ;第 4组 :缺血预调 +格列本脲组 (10 μmol/L) ;第 5组 :腺苷 (2 0 μmol/L) +格列本脲组 (10 μmol/L) ;第 6组 :对照 +格列本脲组 (2 0 μmol/L)。 结果　与对照组相比 ,缺血预调和腺苷可明显改善缺血后心功能恢复 ,减少心肌酶的漏出 ,但此保护作用可被KATP通道阻断剂格列本脲消除。Objective This study was designed to elucidate whether the myocardial protective effects conferred by ischemic preconditioning (IP) or adenosine which was associated with opening of ATP sensitive potassium channels (K ATP channel ). Methods Thirty six isolated buffer perfused rabbit hearts underwent 30 minutes of normothermic potassium arrest followed by 1 hour reperfusion.They were divided into 6 groups: group 1, served as control; group 2, ischemic preconditioning; group 3, treated with adenosine(20 μmol/L); group 4, IP + glibenclamide (10 μmol/L); group 5, adenosine (20 μmol/L)+glibenclamide (10 μmol/L); group 6, control+glibenclamide(10 μmol/L). Results I.P. or adenosine significantly improved the cardiac function and reduced the leakage of myocardial enzymes as compared with that of the control group. Conclusion The beneficial effects of both IP and adenosine were strengthened by K ATP channels which play an important role in the protective effects of IP and adenosine on the myocardium.

关 键 词：KATP通道 缺血预调 作用机制 实验研究 心肌缺血 

分 类 号：R363[医药卫生—病理学]