目的　探讨肠黏膜超微结构改变在急性重症胰腺炎时肠黏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 )观察。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 Objective To investigate the significance of intestinal mucosal ultrastructural changes in intestinal mucosal barrier dysfunction in patients with acute severe pancreatitis. Methods Intestinal mucosa tissues of rats with acute severe pancreatitis (ASP) and sham operation group (SO) were harvested at 6 and 12 h after operation for light microscopy and electron microscopy (horseradish peroxidase was used as mucosal permeability change Of tracer) observed. At the same time, bacterial culture and identification of blood, mesenteric lymph nodes (LMN), liver, spleen and lung tissues were performed to determine the level of endotoxin in portal vein blood. Results The histological changes of intestinal mucosa at 6h and 12h in ASP rats were basically normal. High electron density was observed in the tight junctions of intestinal epithelial cells 12h after electron microscopy. The tight junctions of intestinal mucosal epithelial cells in sham operation group were intact , Cell-free tracer calm. At 12h, the bacterial translocation rate in distal part of ASP group was significantly increased compared with that in sham operation group. The bacteria that were cultured were Escherichia coli, Pseudomonas aeruginosa, Proteus bacillus, Bacillus subtilis, Klebsiella pneumoniae and almost All of them were enterogenous bacteria. Compared with SO group, the level of plasma endotoxin in ASP group significantly increased at 12h. Conclusion Intestinal mucosal epithelial cells are closely connected and open, and the increased permeability is the morphological basis of early intestinal bacteria, endotoxin translocation and intestinal mucosal barrier dysfunction