肺缺血再灌注损伤后TNF IL

向明章　蒋耀光　王如文　范士志　牛会军

　　摘要　为探讨炎性细胞因子在肺缺血再灌注损伤发病机制中的作用，采用大鼠在体温缺血再灌注模型，动态测定了肺组织和血浆肿瘤坏死因子α(TNFα)、白介素-6(IL-6)和白介素-8(IL-8)含量的变化。结果表明，肺缺血再灌注损伤早期肺组织TNFα、IL-6、IL-8相继释放增加，上述因子的血浆变化滞后于肺组织变化。提示炎性细胞因子参与了肺缺血再灌注损伤的发生和发展过程。
　　关键词　肺缺血再灌注损伤　细胞因子

The Changes of TNFα,IL-6 and IL-8 in Lung and Plasma
in Rats With Lung Ischemia-reperfusion Injury and Their Singificances

Xiang Mingzheng,et al.Department of Thoracic Surgery,
The Xinqiao Hospital of Third Militarty medical University,
Chongqing 400037

Abstract To investigate the role of inflammatory cytokines in the pathogenesis of lung ischemia-reperfusion injury,the rat ischemia model with occlusion of left hilus for 45-minute was set up and the changes of levels of TNFα,IL-6 and IL-8 in lung tissues and plasma were dynamically observed during lung ischenia-reperfusion. The results showed that the releases of TNFα,IL-6 and IL-8 in lung tissues were successively increased in the early stage of lung damage and the alterations of above-mentioned cytokines in plasma lagged those in lung tissues. It is concluded that inflammatory cytokines could participated in the onset and development of lung ischemia-reperfusion injury.
Key wards Iung ischemia-reperfusion injury　cytokine

　　肺缺血再灌注损伤是引起早期肺功能障碍的重要原因。近年来，有关急性肺损伤以及细胞因子的许多研究深化了对肺缺血再灌注损伤发病机制的认识。本研究采用大鼠肺在体温缺血再灌注模型，观察了损伤大鼠早期肺组织和血浆TNFα、IL-6和IL-8的变化，探讨其在肺缺血再灌注损伤发病中的作用。
材料与方法
1　动物模型与分组：健康Wistar大鼠，体重200～250g，雌雄不拘。30%戍巴比妥钠40mg/kg B.W腹腔麻醉，气管切开、插管接呼吸机控制呼吸，右颈动脉、静脉插管分别接水银检压计和微泵，经左第五肋间开胸，游离左肺门，静脉注射50u肝素5分钟后于吸气末用无创血管夹阻断左主支气管、左肺动脉和左肺静脉，45分钟后开放行再灌注［1］。48只大鼠随机分为：①损伤组(IRn=24)：肺门游离后夹闭阻断，继行再灌注；②手术对照组(SOn=24)：肺门游离后不夹闭阻断。实验期间按4ml/kg B.W/h经微泵补人林格氏液。各组分4个时组点各处死6只动物，留取标本。
2　肺组织及血浆TNFα、IL-6和IL-8含量：采用放免法检测TNFα、IL-6和IL-8均采用酶联免疫吸附法测定。Lowry法测定蛋白质浓度。
3　统计学处理：数据以±S表示，采用t检验。以P<0.05为差异显著，P<0.01为差异非常显著。
结果
1　肺组织和血浆TNFα含量变化，见表1。IR组肺组织各时相TNF&alpha

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