急性重症大鼠胰炎大鼠肠黏膜超微结构的改变

目的 探讨肠黏膜超微结构改变在急性重症胰腺炎时肠膜屏障功能障碍中的意义。方法 对急性重症胰腺炎（ASP）模型大鼠及假手术组大鼠（SO）于术后6、12h取回肠黏膜组织进行光镜及电镜（利用辣根过氧化酶作为黏膜通透性改变的示踪剂）。同时对血、肠系膜淋巴结（LMN）、肝、脾、肺组织进行了细菌培养及鉴定，测定门静脉血中内毒素水平。结果 ASP大鼠6及12h时相点肠黏膜组织结构基本正常；电镜观察制膜12h肠上皮细胞紧密连接间有高密度电子物质沉着，细胞紧密连接开放；假手术组肠黏膜上皮细胞紧密连接完整，细胞间隙无示踪剂沉着。12h时相点ASP组大鼠远隔部位细菌移位率较假手术组显著增加，培养出的细菌为大肠杆菌、绿脓杆菌、变形杆菌、芳香杆菌、枯草杆菌及肺炎克雷伯杆菌，几乎均为肠源性细菌；12h时相点ASP组大鼠血浆内毒水平较SO组显著增加。结论 肠黏膜上皮细胞间紧密连接开放，通透性增加是ASP早期肠道细菌、内毒素移位，肠黏膜屏障功能障碍的形态学基础。

Significance of gut mucosal ultrastructure changes in the gut mucosal barrier dysfunction in acute severe pancreatitis

Objective To investigate the significance of gut mucosal ultrastructure change in the gut mucosal barrier dysfunction in acute severe pancreatitis(ASP)in rat Methods Ileurn mucosal tissues were studied under microscope and electron microscope (horseradish peroxidase served to trace the gut mucosal permeability) after 6,12 hours of operation in sham and ASP rats respectively.Sampls from blood,ascites and MLN,liver,spleen,pancreas and lung were cultured for bacteria and identification.Plasma LPS level in portal venous blood were measured.Results Gut mucosal morphology were momal in ASP group at 6 and 12 hours.High dense substance could be seen in the tight junction.Cell tight junction opened in ASP group at 12 hours under electron microscope.There were no trace in the gut cell gap in SO group.The bacterial translocation was significantly higher than that in SO group.The bacterial translocated were Escherichia Coli.Pseudomonas aeruginosa.Proteus,Bacillus Subtilis and Klebsiella Pneumoniae,almost all of them were enteric in origin,the level of LPS in ASP group were higher than that in SO group at 12 hours.Conclusion Ultrastructure changes of gut mucosal including enlarged cell gap,opened tight junction,Increased permeability are the morphorlogy basis of gut mucosal barrier dysfunction,bacterial and endotoxin translocation.