目的 :制备肠源性感染致早期肺损伤的动物模型 ,并探讨其作用机制。方法 :采用大鼠盲肠结扎并穿孔 (CL P)造成腹腔感染。分别在术后 0、2 4、48、72、96、12 0小时处死一组大鼠 ,检测肺毛细血管通透性、肺湿 /干比值 ,取支气管肺泡灌洗液 (BAL F)进行细胞学分析 ,检测血浆、肺组织和 BAL F的内毒素和肿瘤坏死因子(TNF)。结果 :肺毛细血管通透性、肺湿 /干比值和 BAL F的中性粒细胞百分率逐渐增加 ,时间越长越明显。血浆、肺组织和 BAL F的内毒素逐渐增加 ,三者之间两两显著相关 ;TNF也逐渐增加 ,肺组织和 BAL F的 TNF显著相关 ,两者与血浆的 TNF无明显相关性。结论 :CL P可制备早期肺损伤的动物模型。肠源性感染导致肺组织中内毒素增加、中性粒细胞积聚、TNF释放 ,肺产生炎性反应 OBJECTIVE: To prepare an animal model of early lung injury caused by intestinal infection and to explore its mechanism. Methods: Intraperitoneal infection was induced by cecal ligation and perforation (CL P) in rats. One group of rats were sacrificed at 0, 2, 44, 48, 72, 96 and 120 hours after operation respectively. The pulmonary capillary permeability and lung wet / dry ratio were measured. BALF was performed on the cells Analysis of the plasma, lung tissue and BAL F endotoxin and tumor necrosis factor (TNF) were detected. Results: Pulmonary capillary permeability, lung wet / dry ratio and BALF neutrophil percentage gradually increased, the longer the more obvious. The endotoxin in plasma, lung tissue and BALF gradually increased. There was a significant correlation between them in every two groups. TNF also increased gradually. There was a significant correlation between TNF and TNF in BALF. There was no significant correlation between them and plasma TNF. Conclusion: CL P can be used to prepare animal models of early lung injury. Gut-derived infections lead to increased endotoxin in lung tissue, neutrophil accumulation, TNF release, and inflammatory reactions in the lung