Effect of ammonia on plasma and cerebrospinal fluid amino acids in dogs with and without portacaval anastomoses

Abstract

To elucidate the possible connection between ammonia-induced changes of plasma and cerebrospinal fluid (CSF) amino acid levels and the development of hepatic encephalopathy in dogs, beagle dogs were given an ammonium acetate infusion both before and following portacaval shunt (PCS). During ammonia-induced coma and after recovery in the dogs prior to PCS the plasma and CSF concentrations of most amino acids were decreased. Following PCS the plasma and CSF concentrations of the aromatic amino acids (AAA), phenylalanine and tyrosine, increased and the levels of the branched chain amino acids (BCAA), valine, leucine, and isoleucine, decreased during ammonia-induced coma. The CSF/plasma molar ratio for the AAA exhibited a marked increase after recovery as compared to the value during coma in the Eck-fistula dogs. With respect to the AAA, no correlation was observed between signs of neurologic impairment in the animals and the following parameters: glutamine and methionine levels of CSF, and the plasma molar ratio (Formula: see text). The data obtained do not support the hypothesis that high concentrations of phenylalanine and tyrosine in the brain may be primarily responsible for altered neurotransmission leading to the development of hepatic encephalopathy.

Metabolomics as a diagnostic tool for hepatology: validation in a naturally occurring canine model

“…The reduced ability of the liver to detoxify and excrete waste results in dramatic changes in the levels of a wide range of metabolites. PVA are associated with hyperammonaemia and disturbances in the concentrations of aromatic and branched chain amino acids in the plasma of affected dogs have been reported (Schafer et al, 1985). The disease state is characterized by the development of neurological (dementia, staggering, circling, central blindness, tremors, seizures and coma) and systemic (stunting, poor body condition, polydipsia, polyuria, vomiting and diarrhoea) signs.…”

Ammonia and GABA-ergic neurotransmission: Interrelated factors in the pathogenesis of hepatic encephalopathy

“…3,25 Moreover, this within the range of ammonia levels in the cerebrospinal fluid concept rationalizes treatments for HE that either lower of animal models of hyperammonemia and humans with heplasma ammonia concentrations (e.g., reduction of colonic patic failure. 6,15,40,41 The cerebrospinal fluid ammonia levels sources of ammonia, or administration of sodium benzoate are most representative of the ammonia concentrations to or ornithine) or reduce GABA-ergic tone by ammonia-indewhich the GABA A receptors are exposed in the extracellular pendent mechanisms (e.g., administration of benzodiazepine spaces of the CNS. Ammonia increased the amplitude of the receptor antagonists).…”

Is portal venous outflow better than systemic venous outflow in small bowel transplantation? Experimental study in syngeneic rats

“…The consequences of PCA are equivalent to those of a portocaval shunt [9,11,12] and involve only some degree of liver atrophy and dysfunction because part of the native portal inflow (that from the stomach, spleen, pancreas, and duodenum) is preserved. Several factors contribute to BT in SBT [13] like cold ischemia, preservation damage, ischemia-reperfusion, and modifications of the intestinal barrier after grafting [14,15].…”