BACKGROUND/AIMS: Little is known about the relationship of portal venous pressure to contractility and histological changes in the gallbladder. In this study, we investigated the relationship between portal hypertension and contractility and histological changes in the gallbladder in a hamster cirrhosis model. METHODS: Liver cirrhosis was induced in the hamsters (n = 20) by thioacetamide (TAA). Portal venous pressure was directly measured using a pressure-measuring instrument. The contractility of the gallbladder was appraised by the diameter before and after caerulein treatment. Gallbladder wall thickness and vessel areas in tissues were evaluated in relation to the portal venous pressure. RESULTS: The portal venous pressure, gallbladder wall thickness with submucosal edema and area of vessels in the gallbladder wall in the cirrhosis group were significantly increased compared with those in the control group (n = 20, receiving saline instead of TAA). The gallbladder contraction rate in the cirrhosis group was significantly decreased compared with that in the control group. In the cirrhosis group, there were positive correlations between the portal venous pressure and the gallbladder contraction rate, gallbladder wall thickness, and area of vessels. CONCLUSIONS: In the gallbladders of experimental cirrhotic hamsters, portal hypertension caused dilatation of the vessels as well as submucosal edema, and was an important factor in the increased thickness and reduced contractility of the gallbladder wall.
BACKGROUND/AIMS: Little is known about the relationship of portal venous pressure to contractility and histological changes in the gallbladder. In this study, we investigated the relationship between portal hypertension and contractility and histological changes in the gallbladder in a hamster cirrhosis model. METHODS:Liver cirrhosis was induced in the hamsters (n = 20) by thioacetamide (TAA). Portal venous pressure was directly measured using a pressure-measuring instrument. The contractility of the gallbladder was appraised by the diameter before and after caerulein treatment. Gallbladder wall thickness and vessel areas in tissues were evaluated in relation to the portal venous pressure. RESULTS: The portal venous pressure, gallbladder wall thickness with submucosal edema and area of vessels in the gallbladder wall in the cirrhosis group were significantly increased compared with those in the control group (n = 20, receiving saline instead of TAA). The gallbladder contraction rate in the cirrhosis group was significantly decreased compared with that in the control group. In the cirrhosis group, there were positive correlations between the portal venous pressure and the gallbladder contraction rate, gallbladder wall thickness, and area of vessels. CONCLUSIONS: In the gallbladders of experimental cirrhotic hamsters, portal hypertension caused dilatation of the vessels as well as submucosal edema, and was an important factor in the increased thickness and reduced contractility of the gallbladder wall.