EXPERIMENTAL ATROPHY HYPERTROPHY COMPLEX (AHC) OF THE LIVER - PORTAL-VEIN, BUT NOT BILE-DUCT OBSTRUCTION, IS THE MAIN DRIVING-FORCE FOR THEDEVELOPMENT OF AHC IN THE RAT

Background/Aims: Patients with lobar or segmental impairment of bile f low or of portal venous blood flow frequently develop considerable atr ophy of the area involved, followed by compensatory hypertrophy/hyperp lasia of the non-affected parts, This configuration is termed atrophy/ hypertrophy complex of the liverMethods: In order to analyze the relat ive contributions of bile duct and portal vein obstruction in the path ogenesis of atrophy/hypertrophy complex, we developed a rat model with selective bile duct and/or portal vein ligation of the anterior liver lobes, representing about two thirds of the liver mass, Evolution of total body weights and weights of the different liver lobes were deter mined, and morphometry and functional scintigraphy (hepatoiodida scann ing) were performed immediately after ligation and at 30 h, 4, 8 and 2 8 days postoperatively. Results: The major findings were: 28 days afte r biliary and/or portal ligation there was no difference between the b ody weights of all animals, all ligated animals having compensated an initial body weight loss, Total liver weight remained constant during the whole observation period, while atrophy of the anterior and hypert rophy/hyperplasia of the posterior lobes occurred, A significant atrop hy/hypertrophy complex developed only after selective portal ligation, but not after selective biliary ligation, Morphometrically analyzed h istologic changes after selective biliary ligation were reversible, wh ereas in portally ligated liver lobes a progressive parenchymal destru ction and involution ,vith subsequent impairment of hepatic function o f the concerned lobe were observed. Conclusions: The present findings indicate that impairment of portal venous flow is the major driving fo rce for the development of lobar atrophy in the rat and that atrophy/h ypertrophy complex can be produced in a rodent model. (C) Journal of H epatology.