Jenkins S A, Grandison A, Baxter J N, Day D W, Taylor I, Shields R
J Hepatol. 1985;1(5):489-99. doi: 10.1016/s0168-8278(85)80747-9.
A method of producing cirrhosis consistently in rats by the administration of dimethylnitrosamine (DMNA) is described. Two weeks following the cessation of DMNA treatment there was distortion of the lobular architecture of the liver and some focal nodule formation. This 'pre-cirrhotic' state was accompanied by portal hypertension, biochemical abnormalities and the development of ascites. The mortality 2 weeks after cessation of DMNA was 42%. Twenty-four weeks after DMNA treatment cirrhosis had developed with diffuse nodularity and fibrosis, marked portal hypertension, and accumulation of ascites. There was also a deterioration in liver function, with hypoproteinaemia and jaundice. The overall mortality 24 weeks after the cessation of DMNA treatment had risen to 52%. This model of cirrhosis in the rat may be useful in evaluating the efficacy of drugs in the long-term management of portal hypertension in man.
