The isolated perfused liver of the cirrhotic rat produces greater quantities of ammonia from endogenous sources or from added alanine than do control livers. It also fails to take up ammonia. In these cirrhotic livers ethanol increases ammonia production in the presence of alanine. When cirrhotic rats had received a normal diet for 10 days before perfusion, the output of ammonia from endogenous sources and from added alanine is partially restored to normal. The addition of ethanol in the presence of alanine to the perfusate of these cirrhotic livers then results in an increased rate of production of glutamine rather than of ammonia. A normal diet given these cirrhotic animals restores the uptake of ammonia to that seen in the control animals but, unlike the normal animals, the addition of ornithine increases neither the uptake of ammonia nor the output of urea. In the normal animals this effect of ornithine on the uptake of ammonia is abolished by ethanol. It is concluded that cirrhotic rat liver is a source of endogenous ammonia and that the magnitude of that contribution is modified by diet and by ethanol.