Experimental atrophy/hypertrophy complex (AHC) of the liver: portal vein, but not bile duct obstruction, is the main driving force for the development of AHC in the rat.
OBJECTIVE
Patients with lobar or segmental impairment of bile flow or of portal venous blood flow frequently develop considerable atrophy of the area involved, followed by compensatory hypertrophy/hyperplasia of the non-affected parts. This configuration is termed atrophy/hypertrophy complex of the liver.


METHODS
In order to analyze the relative contributions of bile duct and portal vein obstruction in the pathogenesis 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 determined, and morphometry and functional scintigraphy (hepatoiodida scanning) were performed immediately after ligation and at 30 h, 4, 8 and 28 days postoperatively.


RESULTS
The major findings were: 28 days after biliary and/or portal ligation there was no difference between the body 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 hypertrophy/hyperplasia of the posterior lobes occurred. A significant atrophy/hypertrophy complex developed only after selective portal ligation, but not after selective biliary ligation. Morphometrically analyzed histologic changes after selective biliary ligation were reversible, whereas in portally ligated liver lobes a progressive parenchymal destruction and involution with subsequent impairment of hepatic function of the concerned lobe were observed.


CONCLUSIONS
The present findings indicate that impairment of portal venous flow is the major driving force for the development of lobar atrophy in the rat and that atrophy/hypertrophy complex can be produced in a rodent model.
Schweizer
W
W
Department of Visceral and Transplantation Surgery, University of Bern, Inselspital, Switzerland.
Duda
P
P
Tanner
S
S
Balsiger
D
D
Höflin
F
F
Blumgart
L H
LH
Zimmermann
A
A
D000818:Animals; D001284:Atrophy / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D001835:Body Weight / Q000502:physiology; D002779:Cholestasis / Q000150:complications*; D004195:Disease Models, Animal; D006984:Hypertrophy / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D008026:Ligation; D008099:Liver / Q000473:pathology* / Q000503:physiopathology; D008102:Liver Circulation / Q000502:physiology*; D008297:Male; D009929:Organ Size; D011169:Portal Vein / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar