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作 者:方勇[1] 陈玉林[1] 葛绳德[1] 朱世辉[1] 刘世康[1]
机构地区:[1]第二军医大学附属长海医院烧伤科
出 处:《中华外科杂志》1998年第11期690-693,共4页Chinese Journal of Surgery
摘 要:目的观察比较烧伤血清及烧伤后中性白细胞(PMN)对肺血管通透性的影响,分析PMN粘附及粘附分子CD11b/CD18在该影响中的介导作用。方法应用离体肺灌流技术,通过肺重量增加(LWG)、液体滤过系数(Kf)和通透性表面积乘积(PS)分别观察肺水肿程度、肺血管对小分子物质和大分子物质的通透性。结果烧伤血清能使LWG、Kf和PS明显增加,以Kf增加最为明显;烧伤后PMN也能使Kf和PS增加,以PS增加为明显;用单抗封闭烧伤后PMN膜上CD11b/CD18后,PMN在肺血管内的滞留减少,Kf和PS值增加被抑制,并以PS改变为显著。结论(1)被激活的PMN释放的介质类物质如氧自由基、蛋白酶等物质对肺微血管内皮细胞(PMEC)的损伤作用部分依赖于PMN与内皮细胞的粘附。(2)烧伤后被激活的PMN释放的介质类物质主要介导肺血管对小分子物质通透性的影响。烧伤后PMN与肺微血管内皮细胞(PMEC)的粘附除了使介质类物质的作用放大外,还介导肺血管对大分子物质通透作用。(3)PMN膜上CD11b/CD18分子可能通过与PMEC细胞间粘附分子的结合。Objective To determine the effect of intercellar adhesion molecule (ICAM 1) CD11b/CD18 in burn activated PMN mediated permeability of microvascular in isolated perfused lung. Method Isolated lungs were distributed into 7 groups according to the different contents of perfused fluid: normal perfused fluid, normal rat serum, burn rat serum, normal rat PMN, burn rat PMN, normal rat PMN blocked by monoclonal antibody to adhesion molecule CD11b/CD18 and burn rat PMN blocked by antibody. The extent of isolated lung edema, vascular permeability to small molecules (fluid) and vascular permeability to large molecules(albumin) were expressed by lung weight gain(LWG), fluid filtration coeffecient(Kf) and pulmonary albumin permeability surface area product(PS) respectively. Result Burn serum could increase LWG,Kf PS, so did burn activated PMN. The latter could make PS increase more obviously. Monoclonal antibody to CD11b/CD18 on PMN could obviously decrease PMN sequestration in isolated perfused lung. The protective effect of antibody on increasing LWG and Kf, and particularly PS was demonstrated. Conclusion (1) The effect of mediators from burn activated PMN to EC was mediated by PMN adhesion to EC. (2) Some mediators from burn activated PMN increase mainly the pulmonary vascular permeability to small molecules, and PMN adhesion to EC mediated by CD11b/CD18 may increase directly the permeability to large molecules. (3)Adhesion molecule CD11b/CD18 perhaps have an ability to regulate directly EC by combining its receptor ICAM 1 on EC.
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