肠缺血-再灌流大鼠远隔脏器受损与中性粒细胞粘附扣留的关系  

Distant organ iniury induced bv out ischemia-reverfusion in rats is related to neutrophil activation and seouestration

作　　者：吕艺[1] 盛志勇[1] 黎君友[1] 严鸣[1] 郑玉清[1] 

机构地区：[1]解放军304医院烧伤研究所基础部,北京100037

出　　处：《感染．炎症．修复》2000年第2期90-92,共3页Infection Inflammation Repair

基　　金：全军"九五"重点科研基金(96L053)

摘　　要：目的:研究肠缺血-再灌流过程中PMN聚集、活化在局部及远隔脏器损伤中的作用及机制。方法:检测大鼠肠缺血再灌流后不同时相全血和组织MPO活性、脏器功能、血浆LPS浓度,观察肠静脉血清对PMN上CD11b和CD18表达的影响。结果:全血和组织MPO活性在再灌流后0.5 h大幅度升高,再灌流后1h,全血、小肠和肝组织MPO活性达峰值(P<0.05～P<0.01);肺组织MPO活性于再灌流2h达峰值,再灌流6h仍维持高水平(P<0.01);脏器功能指标的异常在再灌流后1～2h最明显(P<0.05),并与相应组织MPO活性变化正相关。再灌流后肠静脉血清刺激PMN上CD11b和CD18表达增加,分别与肝、肺组织MPO活性变化呈正相关关系(r=0.9852,r=0.9874,P<0.02)。结论:PMN的聚集、活化参与肠缺血-再灌流过程中局部及远隔组织的损伤过程;PMN上粘附分子表达上调是肠缺血-再灌流后PMN聚集、活化的分子机制之一。Objective:To study the potential role of polymorphonuclear(PMN) aggregation and activation in local and distant organ injury after gut ischemia-reperfusion(GI-R) and its mechanism. Methods: Myeloperoxidase (MPO) activity of blood and tissues, organ function parameters and plasma lipopolysaccharide(LPS) concentration were determined. The effect of serum from intestinal venous blood on the expression of CD11b and CD18 on PMN was measured by ELISA. Results:MPO activity markedly increased in blood and tissues at 0.5h post-reperfusion, and reached a peak level at lb post-reperfusion, while pulmonary MPO activity increased late and lasted longer. GI-R resulted in distant organ dysfunction, which was positively correlated to change in MPO activity in corresponding tissues. In vitro experiments it showed that serum obtained at 1h and 2h post-reperfusion could stimulate the expression of CD11b and CD18 on PMN, which positively correlated to increased MPO activity in lungs and liver. Conclusion: PMN aggregated and activated in tissues might be involved in the damage of local and distant organs after GI-R. The up-regulation of CD11b and CD18 on PMN appears to be the major molecular mechanism of PMN aggregation and activation resulted from GI-R.

关 键 词：肠缺血再灌流 脏器功能损伤 中性粒细胞 髓过氧化物酶 粘附分子 

分 类 号：R392[医药卫生—免疫学]