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作 者:冉珂[1] 段开明[2] 邹定全[1] 朱蓉[1] 卢向航[1] 常业恬[1]
机构地区:[1]中南大学湘雅二医院麻醉科,湖南长沙410011 [2]中南大学湘雅三医院麻醉科,湖南长沙410011
出 处:《现代医药卫生》2007年第16期2371-2372,共2页Journal of Modern Medicine & Health
基 金:湖南省自然科学基金项目(NO.03JJY3053)
摘 要:目的:探讨异氟醚预处理延迟相对缺血再灌注心肌的保护作用及其机制。方法:30只健康新西兰雄性大白兔随机分成3组:假手术组(C组)、缺血再灌注组(I/R组)、2.0%异氟醚预处理延迟相组(S组),每组10只。C组仅开胸160min,I/R组行左冠脉阻断40min,再灌注120min,S组吸入2.0%异氟醚2小时,24小时后处理同I/R组。各组分别于左冠脉阻断前20min(T1)、左冠脉阻断20min(T2)、左冠脉阻断40min(T3)、再灌注1小时h(T4)、再灌注2小时(T5)5个时点抽血测血清IL-10水平。再灌注结束后免疫印迹法测心肌Bcl-2表达水平,用伊文思蓝和TTC染色测心肌梗死面积。结果:与I/R组比,S组IL-10水平增高(P<0.05),Bcl-2表达增高(P<0.05),心肌梗死面积减少(P<0.05)。结论:异氟醚预处理延迟相通过上调心肌Bcl-2表达和IL-10生成来减轻缺血再灌注损伤发挥保护作用。Objective: To investigate the protective effect of isoflurane delayed preconditioning on myocardial ischemia reperfusion injury and the potential mechanisms in rabbit. Methods:Thirty New Zealand male white rabbits were randomly assigned to 3 groups: (1) Control group;(2)I/R group;(3)2.0% isoflurane group. Group 3 was exposed to 2.0% isoflurane-100% oxygen for 2 h. Group 1 and group 2 were exposed 2 h to 100% oxygen serving as untreated controls. Twenty-four hours later group 2 and group 3 underwent 40 min of coronary occlusion followed by 2 h of reperfusion. Blood samples were taken from arterial line at 20min before occlusion (T1),20min after ocelusion(T2),40min after occlusion(T3), lh after reperfusion(T4) and 2h after reperfusion(T5) for determination of the plasma level of IL-10. At the end of the reperfusion, infarct size (IS) and area at risk (AAR) were defined by Evans and TTC staining. The heart was harvested and level of the Bcl-2 expression was determined by Western Blot analysis. Results: The Bcl-2 level of group 3 was significantly higher than that of group 2(P〈0.05). Isoflurane significantly(P〈0.05) reduced infarct size(19.7%±2.8% in group 3) of the left ventricular area at risk as compared with control group (37.8%±1.7% in group 2). Group 3 had a higher levels of IL-10 than that of Group 2. Conclusion: Isoflurane can promote Bel-2 expression and increase the IL-10 level during isehemia reperfusion, which may be one of molecular mechanisms of isoflurane delayed preconditioning on eardioproteetion.
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