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作 者:冉珂[1] 段开明[2] 邹定全[1] 卢向航[1] 李锁北[1] 常业恬[1]
机构地区:[1]中南大学湘雅二医院麻醉科,长沙市410011 [2]中南大学湘雅三医院麻醉科
出 处:《中华麻醉学杂志》2009年第9期825-827,共3页Chinese Journal of Anesthesiology
基 金:湖南省自然科学基金资助项目(03JJY3053);湖南省科技厅资助项目(2007FJ3015)
摘 要:目的探讨异氟醚延迟预处理对兔心肌缺血再灌注时αB-晶状体蛋白表达的影响。方法健康雄性新西兰大白兔30只,体重2.0~2.5kg,随机分为3组(n=10):假手术组(S组)吸入纯氧2h,24h后仅动脉下穿线不结扎;心肌缺血再灌注组(IR组)吸入纯氧2h,24h后行心肌缺血再灌注;异氟醚延迟预处理组(I组)吸入2%异氟醚2h,24h后行心肌缺血再灌注。采用结扎左冠状动脉前降支40min,再灌注120min的方法制备心肌缺血再灌注模型。于再灌注120min时采集动脉血样测定血清超氧化物歧化酶(SOD)活性,取心肌组织测定αB-晶状体蛋白及caspase-3的表达水平,计算心肌缺血面积和梗死面积,观察心肌细胞超微结构。结果s组心肌细胞完整,排列整齐,线粒体形态正常,糖原丰富;IR组心肌细胞水肿,心肌纤维排列紊乱,线粒体、内质网膜肿胀,空泡化;I组心肌细胞水肿程度减轻,心肌纤维排列较完整,线粒体轻度肿胀。与IR组比较,I组心肌梗死面积减小,血清SOD活性升高,心肌caspase-3表达下调,αB-晶状体蛋白表达上调(P〈0.05)。结论异氟醚延迟预处理减轻兔心肌缺血再灌注损伤的机制可能与上调心肌αB-晶状体蛋白表达有关。Objective To investigate the effect of isoflurane-induced delayed preconditioning on αB-crystallin expression during myocardial ischemia-reperfusion (I/R) in rabbits. Methods Thirty male New Zealand white rabbits weighing 2.0-2.5 kg were randomly assigned into 3 groups ( n = 10 each) : group I sham operation (group S) ; group II I/R and group III Isoflurane + I/R (group Iso). Myocardial I/R was induced by 40 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion. In group III , 2% isoflurane in 100% 02 was inhaled for 2 h and I/R was produced 24 h later. At the end of 120 min reperfusion, arterial blood samples were taken for determination of serum SOD activity. The animals were then killed and hearts removed for determination of αB-crystallin expression and caspase-3 expression. Infarct size and area at risk were determined by Evan's blue and TFC staining. Myocardial ultrastructure was examined by electron microscopy. Results The infarct size was significantly smaller, serum SOD activity significantly higher, caspase-3 expression significantly lower, and αB-crystallin expression significantly higher in group Iso than in group I/R (P 〈 0.05). Microscopic examination showed less myocardial damage in group Iso than in group I/R. Conclusion The isoflurane-induced delayed preconditioning attenuates myocardial I/R injury possibly through up-regulating αB-crystallin expression in rabbits.
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