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The protective effect of vasopressin deficiency in liver fibrosis in rats with chronic portocaval anastomosis

Liver fibrosis occur in liver diseases and its complications is cause of the increased rate of human mortality. The disease is characterized by the gradual accumulation of scar tissue in the liver parenchyma with decrease in metabolic capacity and liver failure. It is known that arginine vasopressin (AVP) participate in the regulation of the immune responses, including the scarring. However, the effect of how AVP regulates this process is not clear. Here we study the role of the AVP deficiency induced by the neurointermediate pituitary lobectomy (NIL) in rats with chronic anastomosis portocaval (APC) model (sixteen weeks). Groups of young male Wistar rats of 8–10 each were prepared: Sham operated (SHAM), APC, LNI and APC+NIL. Blood, plasma and serum biochemical variables were assessed: prothrombin time (TP), blood NH3, transaminases (TGO and TGP), bilirubins and γ‐Glutamyl Transpeptidase (GGT). Liver histological slides were stained with H‐E, Masson, Sirius Red and PAS. Results showed that in the APC group: the TP, NH3, TGO and TGP, bilirubins and GGT were significantly increased, whereas serum glucose levels, cholesterol, triglycerides, albumin, total proteins and the liver glycogen content where significantly augmented. Comparisons between SHAM and NIL groups did not shown significant differences in all these variables. As compared with the APC, the APC+NIL group developed a significant improvement in all these variables. The liver histopathology showed that the APC group developed a significant increase in fibrosis septa, inflammatory infiltrates and diminution of the glycogen content. The NIL group we do not have available data yet. In the NIL+APC group histology data showed a significant liver regeneration; less fibrosis, disappearance of inflammatory infiltrates and liver glycogen restoration.