Splanchnic and leg exchange of amino acids and ammonia in acute liver failure

Background & Aims: In patients with acute liver failure, hyperammonemia is associated with cerebral herniation, We examined the splanchnic and leg exc hange of amino acids, urea, and ammonia in such patients, Methods: Bedside liver vein catheterization was used in 22 patients after development of hep atic encephalopathy grades Ill-IV. Femoral venous blood was sampled in 7 of these patients. Results: Arterial amino acid concentration (8.1 +/- 4.1 mm ol/L) was increased 4-fold above normal, Glutamine (2.4 +/- 1.8 mmol/L) and alanine (0.57 +/- 0.35 mmol/L) were by far the predominant amino acids exc hanged in the splanchnic and leg circulation. In the splanchnic circulation , there was a net uptake of glutamine (241 +/- 353 mu mol/min) and ammonia and alanine were released in an almost 1:1 stoichiometry (r(2) = 0.47; P < 0.001). In the leg, ammonia and alanine were removed and glutamine released . The leg ammonia concentration difference was correlated to that of glutam ine (r(2) = 0.80; P = 0.008) and alanine (r(2) = 0.67; P = 0.03), Conclusio ns: Splanchnic metabolism of glutamine in combination with decreased hepati c function was responsible for the splanchnic release of ammonia and alanin e, These processes were reversed in skeletal muscle. Stimulation of skeleta l muscle metabolism of ammonia could be a important target for future treat ment of patients with acute liver failure.