腹腔感染实验大鼠肠粘膜屏障功能的变化及机理  

A study on the changes of the functions of the intestinal mucosal barrier and its mechanism in rats with intraperitoneal infection

作　　者：余佩武[1] 蔡志民[1] 曾冬竹[1] 秦孝健[1] 周立新[1] 

机构地区：[1]第三军医大学西南医院普通外科

出　　处：《中华普通外科杂志》1999年第1期56-58,共3页Chinese Journal of General Surgery

摘　　要：目的探讨实验大鼠腹腔感染时肠粘膜屏障功能变化及其发病机理。方法在盲肠结扎加穿孔（ＣＬＰ）模型上，观察肠粘膜通透性、肠粘膜血流量、血浆内毒素、肠道荧光标记菌示踪以及肠组织血小板活化因子（ＰＡＦ）、磷脂酶Ａ２（ＰＬＡ２）和丙二醛（ＭＤＡ）的变化。结果腹腔感染组比对照组肠粘膜通透性和血浆内毒素水平明显升高；肠道荧光标记菌大量移位于肠外器官。肠粘膜血流量明显降低。肠组织ＰＡＦ、ＰＬＡ２和ＭＤＡ水平明显升高。应用ＰＡＦ拮抗剂ＷＥＢ２１７０治疗能明显减轻肠粘膜损害，有效降低肠道细菌移位率和血浆内毒素水平。结论腹腔感染时有肠粘膜屏障功能严重受损和肠源性感染发生。Objective To investigate the changes of the intestinal mucosal barrier and the mechanism in rats with intraperitoneal infection.Methods A rat model of intraperitoneal infection was made by cecal ligation and puncture (CLP) in this experiment.The intestinal mucosal permeability and blood flow,the plasma endotoxin,the fluoresence labelled E coli tracer in gut and the intestinal platelet activating factor (PAF),phospholipase A 2 (PLA 2), malondialdehyde (MDA) were measured.Results The intestinal mucosal permeability and plasma endotoxin level were markedly elevated.Fluorescence labelled E coli in gut translocated to other visceral organs.The intestinal mucosal blood flow was significantly decreased.The level of PAF、PLA 2 and MDA in intestinal tissues were significantly increased.PAF antagonist could evidently alleviate the demage of the intestinal mucosa and decrease the rate of bacterial translocation and the level of plasma endotoxin.Conclusions The intraperitoneal infection causes the injury of intestinal mucosal barrier and leads to gut origin sepsis,and PAF is associated with the pathophysiological changes seen in experimental intraperitoneal infection.

关 键 词：腹腔感染 肠粘膜 屏障功能 PAF 

分 类 号：R656[医药卫生—外科学]