Abstract
In acute metabolic acidosis urinary ammonia excretion and renal glutamine extraction increase; however, arterial glutamine level stays unchanged or rises. This suggests increased glutamine production in some extrarenal organ, and this is what happens. During acute sulfuric acid acidosis in dogs there is increased glutamine production in the liver. In addition to kidney, the intestinal tract normally extracts glutamine from the splanchnic arterial blood, and this increases markedly in acidosis. The arteriovenous glutamine difference across brain varies around zero in the normal dog, but in acidosis there is always increased brain glutamine uptake. The significance of these findings, and the possible feedback system relating hepatic glutamine production to its extrahepatic utilization in normal and acidotic states is discussed.