Open AccessLiver atrophy following portacaval shunt in normal rats: A morphologic and ultrastructural study
Author(s) -
Tatjana Radosavljević,
Vesna Todorovic,
Ivan Boričić,
Branka Šikić
Publication year - 2003
Publication title -
acta veterinaria
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.308
H-Index - 17
eISSN - 1820-7448
pISSN - 0567-8315
DOI - 10.2298/avb0303121r
Subject(s) - portacaval shunt , atrophy , endoplasmic reticulum , pathology , perisinusoidal space , hepatocyte , ultrastructure , biology , cirrhosis , endocrinology , histology , pancreas , medicine , portal hypertension , biochemistry , in vitro
The aim of the current study was to examine morphological and ultrastructural changes in the rat liver in an experimental model of chronic liver disease (end-to-side portacaval shunt). The surgical procedure providing an end-to-side portacaval shunt (PCS) was performed in Wistar rats. The liver and pancreas weights were determined 8 weeks after the operation, when liver histology and ultrastructural patterns of hepatocytes were examined. Body weights were not significantly different between the groups 8 weeks after the operation. Liver weight was significantly lower in PCS rats than in control and sham operated (SHAM) rats. The same was observed when liver weight was expressed as a percentage of body weight. Pancreas weight was significantly greater in PCS than in control and SHAM rats. Liver histology in rats with PCS showed glycogen depletion and sinusoidal dilatation around the hepatic vein. Kupffer's cells were filled with haemosiderin. The hepatocytes surrounding the portal space exhibited degenerative and microvesicular fatty changes. Multiplication of the biliary ductules in the portal space was present. Atrophy of hepatocytes occurred in other parenchymal zones and apoptopic hepatocytes were seen more frequently in rats with PCS. The ultrastructural characteristics of hepatocyte cell lesions in rats with PCS at the end point of our experiment included reduction and fragmentation of rough endoplasmic reticulum with destroyed or dilated cisternae and few polysomes accompanied by proliferation of smooth endoplasmic reticulum. The present study suggests that end-to-side PCS in rats causes liver atrophy and that the morphological and ultrastructural changes in the hepatocytes partially explain the metabolic and endocrine abnormalities