An Experimental Model of Liver Cirrhosis in Laboratory Animals

Abstract

Objective: to develop and justify the application of a new experimental method of the simulation of liver cirrhosis in laboratory animals. Material and methods. The simulation of liver cirrhosis was performed on 11 eugamic white Wistar male rats with the body weight of 203.5 ± 22.2 g (experimental group). The control group consisted of 12 healthy laboratory animals. Acute toxic liver injury resulting in cirrhosis was caused by means of the intraperitoneal administration of 50 % solution of carbon tetrachloride (CCl4) in olive oil on the first day of the experiment at a dosage of 0.1 ml of CCl4 + 0.4 ml of olive oil per 100 g of the body weight of the animals, on the second day of the experiment - 0.3 ml of CCl4 + 0.2 ml of olive oil per 100 g of the body weight of the animals. For synergism and potentiation of the hepatotoxic effect of CCl4, the animals daily had free access to 10% ethanol solution. The duration of the experiment was 65 days. The clinical and laboratory parameters were evaluated, the histological assessment of the preparations was carried out. The obtained data were compared with the same parameters of the control group of the animals. Results. The reproducibility of the model was 81.8% (9 animals). The values of the biochemical blood analysis indicated statistically significant increases in the levels of total bilirubin, serum transaminases (AST, ALT), creatinine, a decrease in the glucose level in the animals of the experimental group. The complex morphological confirmation of liver cirrhosis in progress was obtained. Conclusion. The proposed method of the liver cirrhosis modeling correlate with the values of the biochemical blood analysis, pathological changes in the tissue of the liver and internal organs of liver cirrhosis in humans. With the help of the original model, it is possible to investigate the pathogenesis and effects of various groups of pharmacological drugs on liver cirrhosis and its complications (acute blood loss associated with the syndrome of portal hypertension).