Urea cycle enzymes which broadly control ammonia metabolism in the liver are being investigated after experimental portacaval shunt operations. The shunt operation has received considerable attention from clinicians because it is a definitive treatment for hemorrhage from esophageal varices secondary to portal hypertension. The role of urea cycle enzymes is of particular interest in this situation because of striking changes in ammonia and cerebral metabolism induced by this surgery. There is good evidence that under these conditions there is a close relationship between ammonia utilization and cerebral metabolism,1 but the mechanism for this is not well understood. In this study attention is focused only on one phase, utilization of ammonia by the liver, as a part of a broader over-all study of liver-brain relationships.
Ammonia, commonly thought of in terms of toxicity in hepatic failure and coma, is in point of fact an essential metabolite in the hepatic urea
Brown H, Brown J. Urea Cycle Enzymes After Portacaval Shunting. JAMA. 1965;192(5):382–384. doi:10.1001/jama.1965.03080180040009
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