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结扎Ｗｉｓｔａｒ大鼠胆总管制备胆汁性肝硬化模型。取结扎术后１～８６ｄ不同时间的肝脏，用光学显微镜和电镜观察肝硬化形成过程的病理和超微病理变化。探讨了肝硬化胶原纤维增生和结节形成的机制：胆总管结扎后胆汁郁积造成肝细胞损伤、坏死、激发小胆管样上皮细胞增殖并分化演变，大多数变成小胆管，少数变成小结节状肝细胞。小胆管样上皮细胞和小胆管上皮细胞具有合成胶原纤维的能力。增殖的小胆管、纤维母细胞、毛细血管等和伴随其增生的胶原纤维一起形成结缔组织，隔包围、分割、改建原来的肝小叶而形成假小叶，终于导致肝硬化形成。
Preparation of bile cirrhosis model by ligating the common bile duct of Wistar rats. The livers were taken from 1 to 86 days after ligation, and pathological and ultrastructural changes of liver cirrhosis were observed by light microscope and electron microscope. The mechanism of hepatic cirrhosis collagen fibrosis and nodule formation was discussed. Cholestasis caused by cholestasis in the common bile duct resulted in hepatocyte injury and necrosis, which stimulated the proliferation and differentiation of small bile duct epithelial cells. Most of them became small bile ducts and few became nodules Day-like hepatocytes. Small bile duct-like epithelial cells and small bile duct epithelial cells have the ability to synthesize collagen fibers. Proliferation of the small bile duct, fibroblasts, capillaries and other accompanied with hyperplasia of collagen fibers together to form connective tissue, surrounded by separation, reconstruction of the original hepatic lobules and the formation of false lobules, and finally lead to the formation of cirrhosis.