Hyperammonemia following ureterocolostomy in the rat.

Following ureterosigmoidostomy, encephalopathy with hyperammonemia may occur in the presence of cirrhosis, and the same complication was also observed in a few patients without liver damage. This suggests overloading of normal liver ureagenisis by an increased portal ammonia supply. To test this hypothesis and to try to produce an experimental model of chronic hyperammonemia without portal or hepatic damage, ureterocolostomies were performed in rats. These rats were compared with sham operated upon rats and with rats having chronic uremia induced by subtotal nephrectomy. Rats having a ureterocolostomy had chronic, but moderate, systemic hyperammonemia without any histologic hepatic damage and without gross behavioral modifications and slight uremia with only inconstant pyelonephretic lesions. In these rats, hyperammonemia results from hepatic overloading by the increased portal ammonia supply which is a consequence of both intestinal absorption of some urinary ammonia and increased intestinal ammoniagenesis induced by hydrolysis of urinary and circulating urea.