Amino Acid Disturbances in Experimental Hepatic Coma Rats

Abstract

In our previous paper (1), we discussed the in-vitro adsorption spectrum of plasma amino acids by coated charcoal hemoperfusion. We now describe the general amino acid disturbances in plasma, CSF and cerebrum in the galactosamine induced hepatic coma model in rats. All aromatic amino acids (AAA) increased significantly in the three compartments studied. Branched chain amino acids (BCAA) were either elevated to a much lesser extent or remained unchanged. The molar ratio of BCAA:AAA was consequently reduced. This is similar to findings in fulminant hepatic failure in human and other animal models. Most of the 20 amino acids analyzed were increased significantly in the plasma. Increases of amino acids were minimal in the brain tissue studied, i.e. the cerebrum.

Brain lactate by magnetic resonance spectroscopy during fulminant hepatic failure in the dog

“…Intracranial hypertension was an important finding in our study, although no evidence of edema was observed on gross or microscopic examination of the brain in the study of Diaz-Buxo et al 44 A higher dose of 1.7-2.0 g/kg of D-galactosamine may be needed in the dog for the formation of cerebral edema. The development of cerebral edema and intracranial hypertension after infusion of D-galactosamine is supported by past reports using rats 36,45,46 and rabbits. 47,48 Although the current study was conducted in an experimental facility at 9.4 T, observations made in this study regarding brain lactate are transferable to the clinical setting.…”

“…supported by past reports using rats 36,45,46 and rabbits. 47,48 Although the current study was conducted in an experimental facility at 9.4 T, observations made in this study regarding brain lactate are transferable to the clinical setting.…”

Study of Carnitine/Acylcarnitine and Amino Acid Profile in Children and Adults With Acute Liver Failure

“…ALF causes marked, but nonspecific hyperaminoacidemia (41)(42)(43)(44)(45), attributed to hepatocellular damage with leakage of intracellular amino acids into the circulation (41). In most patients, this hyperaminoacidemia involves either those amino acids with high intracellular concentrations (glutamine, glutamate, alanine, glycine, lysine, threonine, and histidine) or those metabolized predominantly in the liver (phenylalanine, tyrosine, and methionine) (41).…”