Pathogenesis of hepatic atrophy in canine model of hepatolithiasis.

The pathogenesis of the hepatic atrophy that accompanies hepatolithiasis was investigated pathomorphologically using a canine model. Two groups were evaluated: infected and noninfected. In the infected group, inflammation in Glisson's capsule caused by cholangitis involved the portal vein at the region of the large bile duct. At this region, the periportal fibrosis ratio was significantly greater in the infected group than in the noninfected group both at 1 and 3 months. At the regions of the septal and interlobular bile ducts, the caliber ratio of the portal vein in the two experimental groups was less than in the normal liver both at 1 and 3 months. At both regions, the caliber ratio of the portal vein in the infected group was less than in the noninfected group at 3 months. The rate of atrophy was significantly greater in the infected group than in the noninfected group at 3 months. These results suggest that disturbance of the portal venous blood flow attributed to cholangitis of the large bile ducts is one of the most important factors leading to hepatic atrophy in hepatolithiasis.