Effects of acute metabolic acidosis on renal, gut, liver, and muscle metabolism of glutamine and ammonia in the dog

Abstract

Previous studies have shown a rise in arterial glutamine in acute acidosis in the dog. In these experiments glutamine and ammonia metabolism was studied in anesthetized dogs during normal acid-base status and following acute hydrochloric acidosis to determine the mechanism for the rise in arterial glutamine in acidosis. Splanchnic, liver, renal, and hind-half extraction/production were measured by arteriovenous (a-v) sampling and simultaneous blood flow measurements using electromagnetic flow probes. In the normal dog, muscle produced glutamine, and the kidneys, gut, hepatosplanchnic bed, and liver extracted it. Whole blood arterial glutamine rose in acidosis. Renal and muscle glutamine and ammonia extraction/production were unchanged. Gut ammonia release and hepatic ammonia uptake increased by similar amounts in acidosis, but no change in gut glutamine uptake occurred. Hepatic and total hepatosplanchnic glutamine uptake was markedly thereby contributing to the raised arterial glutamine. These results demonstrate that acute metabolic acidosis in the dog influences marked changes in glutamine extraction and ammonia metabolism across the hepatosplanchnic bed without significant changes in kidney or muscle metabolism.