Influence of hepatic ammonia removal on ureagenesis, amino acid utilization and energy metabolism in the ovine liver.

The mass transfers of O2, glucose, NH3, urea and amino acids across the portal-drained viscera (PDV) and the liver were quantified, by arterio-venous techniques, during the last 4 h of a 100 h infusion of 0 (basal), 150 or 400 mumol NH4HCO3/min into the mesenteric vein of three sheep given 800 g grass pellets/d and arranged in a 3 x 3 Latin-square design. Urea irreversible loss rate (ILR) was also determined by continuous infusion of [14C]urea over the last 52 h of each experimental period. PDV and liver movements of glucose, O2 and amino acids were unaltered by NH4HCO3 administration, although there was an increase in PDV absorption of non-essential amino acids (P = 0.037) and a trend for higher liver O2 consumption and portal appearance of total amino acid-N, glucogenic and non-essential amino acids at the highest level of infusion. PDV extraction of urea-N (P = 0.015) and liver removal of NH3 (P < 0.001), release of urea-N (P = 0.002) and urea ILR (P = 0.001) were all increased by NH4HCO3 infusion. Hepatic urea-N release (y) and NH3 extraction (x) were linearly related (R2 0.89), with the slope of the regression not different from unity, both for estimations based on liver mass transfers (1.16; SE 0.144; P(b) not equal to 1 = 0.31) and [14C]urea (0.97; SE 0.123; P(b) not equal to 1 = 0.84). The study indicates that a sustained 1.5 or 2.4-fold increase in the basal NH3 supply to the liver did not impair glucose or amino acid supply to non-splanchnic tissues; nor were additional N inputs to the ornithine cycle necessary to convert excess NH3 to urea. Half of the extra NH3 removed by the liver was, apparently, utilized by periportal glutamate dehydrogenase and aspartate aminotransferase for sequential glutamate and aspartate synthesis and converted to urea as the 2-amino moiety of aspartate.