Kono K, Ohnishi K, Omata M, Saito M, Nakayama T, Hatano H, Nakajima Y, Sugita S, Okuda K
First Department of Medicine, Chiba University School of Medicine, Japan.
Gastroenterology. 1988 Mar;94(3):787-96. doi: 10.1016/0016-5085(88)90255-7.
An attempt was made to develop an animal model for the study of the etiology of noncirrhotic portal fibrosis or idiopathic portal hypertension based on the assumption that it is related to chronic abdominal infection. Rabbits were given killed nonpathogenic Escherichia coli intraportally or intravenously. The animals to which a mixture of killed E. coli and rabbit antiserum (aggregated E. coli) was given intraportally developed remarkable histologic changes in the liver. The early inflammatory reactions in the portal area and parenchyma were followed by rapid disappearance of inflammation and development of portal fibrosis with bile duct proliferation. Three intraportal challenges with aggregated E. coli were sufficient to produce pronounced portal fibrosis, although there was considerable variation in response among individual animals. This procedure also produced splenomegaly, and in some animals marked portal hypertension. Injection of nonaggregated killed E. coli into the portal vein or aggregated E. coli into the ear vein also caused similar hepatic changes, but they were milder in degree. These histologic changes resemble portal fibrosis seen in idiopathic portal hypertension and, less closely, pericholangitis associated with inflammatory bowel disease in humans.
基于非肝硬化性门脉纤维化或特发性门脉高压的病因与慢性腹部感染有关这一假设，人们尝试建立一种动物模型用于该病因的研究。给兔子经门静脉或静脉注射灭活的非致病性大肠杆菌。经门静脉给予灭活大肠杆菌与兔抗血清混合物（聚集的大肠杆菌）的动物，肝脏出现了显著的组织学变化。门脉区和实质的早期炎症反应之后，炎症迅速消退，门脉纤维化伴胆管增生逐渐发展。尽管个体动物的反应存在相当大的差异，但经门静脉三次注射聚集的大肠杆菌足以产生明显的门脉纤维化。该操作还导致脾脏肿大，在一些动物中出现明显的门脉高压。将未聚集的灭活大肠杆菌注入门静脉或把聚集的大肠杆菌注入耳静脉也会引起类似的肝脏变化，但程度较轻。这些组织学变化类似于特发性门脉高压中所见的门脉纤维化，与人类炎症性肠病相关的胆管周围炎的相似程度稍低。
