title: Liver impairment after portacaval shunt in the rat: the loss of protective role of mast cells?
abstract: Mast cells are involved in various liver diseases and appear to play a broader pathogenic role than originally thought. They may participate in the splanchnic alterations related to a porto-systemic shunt. To verify this hypothesis we studied the serum and hepatic histological changes in rats four weeks after an end-to-side portacaval shunt. In this experimental model of chronic liver insufficiency we also assessed the mucosal mast cells (MMC) and connective tissue mast cells (CTMC) in the liver, mesenteric lymph nodes and small intestine, as well as the serum levels of rat mast cell protease-II (RMCP-II). The results show liver and testes atrophy, with hypoalbuminemia (p=0.0001), hyperbilirubinemia (p=0.0001) and increase in aspartate aminotransferase (p=0.004) and alanine aminotransferase (p=0.0001). Hepatic histopathology demonstrates hepatocytic necrosis and apoptosis, portal inflammation, biliary proliferation, steatosis and fibrosis. There is a decrease of MMCs and CTMCs in the liver, while in the ileum CTMCs increase and MMCs decrease. These results suggest the involvement of mast cells in the pathophysiological splanchnic impairments in this experimental model. In particular, the decreased number of liver mast cells may be associated with the hepatic atrophy. If this is the case, we propose that the disruption of the hepato-intestinal axis after a portocaval shunt in the rat could inhibit the ability of the liver to developing an appropriate repair response mediated by mast cells.
authors.affiliation: Department of Surgery I, School of Medicine, Complutense University of Madrid, Spain. maaller@med.ucm.es
authors.forename: Maria-Angeles
authors.initials: MA
authors.lastname: Aller
authors.forename: Vicente
authors.initials: V
authors.lastname: Martinez
authors.forename: Maria-Teresa
authors.initials: MT
authors.lastname: Corcuera
authors.forename: Javier
authors.initials: J
authors.lastname: Benito
authors.forename: Estefania
authors.initials: E
authors.lastname: Traver
authors.forename: Fernando
authors.initials: F
authors.lastname: Gómez-Aguado
authors.forename: Patri
authors.initials: P
authors.lastname: Vergara
authors.forename: Jaime
authors.initials: J
authors.lastname: Arias
mesh_terms: D000410:Alanine Transaminase / Q000032:analysis; D000818:Animals; D001219:Aspartate Aminotransferases / Q000032:analysis; D002452:Cell Count; D002908:Chronic Disease; D053818:Chymases / Q000032:analysis; D003239:Connective Tissue Cells / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D048550:Hepatic Insufficiency / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D007413:Intestinal Mucosa; D008099:Liver / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008103:Liver Cirrhosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D008198:Lymph Nodes / Q000378:metabolism / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000473:pathology*; D008643:Mesentery / Q000378:metabolism / Q000473:pathology; D009092:Mucous Membrane / Q000378:metabolism / Q000473:pathology; D009336:Necrosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D011167:Portacaval Shunt, Surgical / Q000009:adverse effects*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; C083294:chymase 2; D053818:Chymases