腹部创伤感染时胃肠粘膜屏障损害的实验研究

目的：探讨腹部创伤感染时胃肠粘膜屏障损害过程及其发病机制．方法：在盲肠结扎加穿孔（ＣＬＰ）模型上，进行胃肠粘膜电位（ＰＤ）、血流量，肠粘膜通透性，血浆内毒素和血小板活化因子（ＰＡＦ）含量测定以及荧光标记菌示踪和组织形态学等观察．结果：腹腔感染大鼠胃肠粘膜ＰＤ和血流量显著降低；肠粘膜通透性和血浆内毒素水平显著升高；肠道荧光标记菌大量移位于肠外器官．血ＰＡＦ水平也显著升高，且与胃肠粘膜损害程度呈一致性相关．而应用ＰＡＦ拮抗剂ＷＥＢ２１７０治疗能明显减轻胃肠粘膜病理损害和降低肠道细菌移位率．结论：腹部创伤后腹腔感染时胃肠粘膜屏障出现广泛损伤和肠源性感染发生，而ＰＡＦ是导致这一病理生理改变的重要因素之一．

An Experimental Study of Gastrointestinal Mucosal Barrier Injury in Abdominal Trauma and Infection

Aim: To investigate the injurious processes in the gastrointestinal mucosal barrier and its mechanism in abdominal trauma and infection. Methods: A model of cecal ligation and puncture (CLP) of rat was used in this experiment. The gastrointestinal mucosal potential difference (PD), blood flow and intestinal mucosal permeability and the content of plasma endotoxin and platelet activating factor (PAF) were measured. Fluorescence labelled B. coli trace and cellular structures were observed. Results: In CLP animals, the gastrointestinal mucosal PD and blood flow were significantly decreased. The intestinal mucosal permeability and plasma endotoxin were markedly elevated. A lot of the fluorescence labelled B.coli in gut translocated to other visceral tissues. The level of blood PAF was also significantly increased and the change was positively correlated with injurious severity of the gastrointestinal mucosa. To treat CLP animals with PAF antagonist could evidently alleviate the pathological injury of gastrointestinal mucosa and decrease the rate of bacterial infection. Conclusion: The intraperitoneal infection after abdominal trauma can cause the injury of gastrointestinal mucosal barrier and induce gut origin sepsis, and PAF is one of the important factors causing the pathophysilogical changes.