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Brain Quinolinic Acid in Chronic Experimental Hepatic Encephalopathy: Effects of an Exogenous Ammonium Acetate Challenge
Author(s) -
Bergqvist Peter B. F.,
Heyes Melvyn P.,
Bugge Mogens,
Bengtsson Finn
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.65052235.x
Subject(s) - quinolinic acid , medicine , hepatic encephalopathy , neurotoxin , endocrinology , glutamate receptor , agonist , coma (optics) , encephalopathy , chemistry , ammonium acetate , receptor , biochemistry , cirrhosis , high performance liquid chromatography , tryptophan , amino acid , chromatography , physics , optics
Elevated brain concentrations of the neurotoxin and NMDA receptor agonist quinolinic acid (QUIN) have been demonstrated in portacaval‐shunted (PCS) rats, a chronic hepatic encephalopathy (HE) model. Increased brain QUIN levels have also been shown in acute hyperammonemic rats. In the present study, the plasma and brain (neocortical) QUIN levels in chronic PCS rats were investigated. The study also included a single exogenous ammonium acetate (NH 4 Ac; 5.2 mmol/kg, i.p.) challenge to precipitate a reversible hepatic coma. Compared with sham‐operated controls, chronic PCS rats exhibited decreased rather than increased plasma and brain QUIN levels. The plasma‐to‐brain QUIN ratio was not found to be altered. The NH 4 Ac administration induced coma in all of the PCS rats 20–25 min after the challenge, and this coma was resolved within 60–75 min. No relevant temporal relationship between changes in brain QUIN levels and the neurological status in the PCS rats was observed. Therefore, our results do not support the contention that increased brain QUIN levels per se are involved in the pathogenesis of HE.