Objective:To investigate the effects of isoflurane preconditioning on apoptosis of immature myocardial cells and the expression of ICAM-1 and NF-KB after ischemia reperfusion in immature rabbits. To discuss the protective mechanism of isoflurane against ischemia-reperfusion injury of immature myocardial cell. Methods: 32 Japanese Big-ear rabbits were randomly divided into four groups: The sham operation group,the heart were exposed ,but the coronary artery were not ligatured;The ischemia-reperfusion group:the left anterior descending coronary artery were ligatured 30 min, then followed by 2 hour reperfusion;The isoflurane preconditioned group : the rabbits were treated with isoflurane(1. 1 ％) 30 min before ischemia. In the gliben clamide group: the rabbits were treated with gliben clamide (O. 5mg/kg) before breathing in isoflurane. Apoptosis of myocardial cells were detected by TUNEL method,the expression of ICAM-1 and NF-KB were examined by immunohistochemical technique,and the fine cells in isoflurane group and fake operation group were observed under electron microscope as well. Results: The apoptosis of myocardial ischemiareperfusion group and gliben clamide group(P＜0. 05). The expression of ICAM-1 and NF-κB were significantly lower than those in ischemia-reperfusion and gliben clamide group(P＜0. 05). The injury extent of isoflurane group was smaller than that in ischemia-reperfusion and gliben clamide group seen from the changes of the celluar structure under electron microscope. Conclusion: Isoflurane can decrease apoptosis of myocardial cells induced by ischemia-reperfusion,lsoflurane preconditioning may provide obviously myocardial protection against ischemia-reperfusion injury in immature rabbit heart, by decreasing the expression of ICAM-1、NF-κ and K-ATP channels is likely involved in this protective mechanism.%目的:探讨异氟醚对幼兔缺血再灌注心肌细胞间黏附分子-1,NF-κB的影响及其对心肌缺血再灌注保护的作用机制.方法:取32只日本大耳白幼兔随机分为4组,假手术组只穿线不结扎;缺血再灌注组:结扎30 min,再灌注2h;异氟醚预处理组:缺血前吸入1.1%异氟醚30 min,洗脱15min后处理同缺血再灌注组;格列苯脲组:异氟醚吸入前于耳缘静脉注射格列苯脲0.5mg/kg后处理同异氟醚预处理组.观察心肌细胞凋亡和细胞间黏附分子-1,NF-κB蛋白表达情况,电镜观察超微结构.结果:异氟醚预处理组细胞凋亡较缺血再灌注组和格列苯脲组明显减少(P＜0.05),异氟醚预处理组细胞间黏附分子-1,NF-κB的表达明显较缺血再灌注组和格列苯脲组低(P＜0.05),电镜显示异氟醚预处理组细胞损伤程度小于缺血再灌注组和格列苯脲组.结论:异氟醚预处理对幼兔缺血再灌注心肌损伤有明显的保护作用,其机制通过下调细胞间黏附分子-1,NF-κB蛋白表达并与促K+ATP通道开放有关.
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