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延迟预适应对缺血再灌注损伤冠状动脉内皮细胞的保护作用 被引量:1

Protective Effects of Delayed Ischemic Preconditioning on Ischemia/Reperfusion Injury in the Coronary Endothelial Cells
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摘要 目的:研究延迟缺血预适应(IPC)对缺血再灌注(I/R)冠状动脉内皮细胞的保护作用。方法:所有动物随机分为三组:假手术组(CON组,n=6),缺血再灌注组(I/R组,n=6),预适应组(IPC组,n=6)。I/R组及IPC组分别于不同时间段抽血检测NO、丙二醛(MDA)及超氧化物歧化酶(SOD)的含量。实验结束后,取心脏左前降支(LAD)所支配的心肌组织一小块,行免疫组化染色。结果:IPC组NO缺血前明显高于开胸后,缺血前IPC组高于I/R组;MDA含量缺血前及再灌注后IPC组均低于I/R组;SOD的活性,再灌注后两组差异显著。IPC组内皮型一氧化氮合成酶(eNOS)的表达明显高于I/R组。结论:延迟预适应早期内皮细胞生成NO的量增加,自由基减少,且保护后期的再灌注中NO、自由基的量处于相对稳定,同时使内皮中SOD的活性及eNOS的表达增加。 Objective: To study the protective effects of delayed ischemic preconditioning on coronary endothelial function after ischemia/reperfusion.Method: All rabbits were divided randomly into three groups: Control group (CON group, n=6), ischemia/reperfusion group(I/R group, n=6) and ischemic preconditioning group (IPC group, n=6). In I/R group and IPC group, blood samples were taken for analysing the changes of the content of NO, MDA and SOD in not meantime the segment. At the end of experiment, sliced little myocardium supplied with LAD to study the expression of eNOS with immunohistochemistry.Results: NO increased significantly before ischemia than after opening thorax in IPC group. Compared with after opening thorax, NO of IPC group was higher than that of I/R group. The level of MDA in IPC group was lower than that in I/R group after reperfusion and before ischemia. After reperfusion, the level of SOD in IR group was markedly decreased, but that of IPC group was significantly enhanced. For the expression of eNOS, that of IPC group was higher than that of IR group.Conclusion: Delayed IPC increases the release of NO and reduses the free radicals in the early phase, and preserves appropriate level of NO and free radicals during reperfusion, meanwhile, IPC improves the activity of SOD and increases the expression of eNOS in coronary endothelial cells.
出处 《微循环学杂志》 2006年第1期23-25,F0004,共4页 Chinese Journal of Microcirculation
关键词 缺血再灌注损伤 延迟预适应 保护作用 冠状动脉内皮细胞 心脏缺血再灌注 缺血预适应 早期预适应 生理现象 I/R 时间段 Delayed ischemic preconditioning Free radical Nitric oxide synthase Endothelial cells
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