Toxins in hepatic encephalopathy: the role of the synergistic effect of ammonia, mercaptans and short chain fatty acids.
Evidence has been recently produced that neurological changes which characterize hepatic encephalopathy due to fulminant hepatic failure in rats are linked with a pathology of GABA receptors. In the search for the peripheral toxins responsible for the CNS impairment present in hepatic encephalopathy it has been shown that the administration of ammonia and mercaptans and octanoic acid in normal rats reproduced behavioural and electrophysiological changes similar to those seen in galactosamine induced encephalopathy. The present report shows that a subacute administration of the above toxins induced a marked alteration of the GABA receptor complex which may account for the CNS derangement of hepatic encephalopathy.
D000641:Ammonia / Q000633:toxicity*; D000818:Animals; D002210:Caprylates / Q000633:toxicity*; D004357:Drug Synergism; D006501:Hepatic Encephalopathy / Q000139:chemically induced / Q000503:physiopathology*; D007700:Kinetics; D051381:Rats; D011963:Receptors, GABA-A / Q000187:drug effects / Q000378:metabolism; D013438:Sulfhydryl Compounds / Q000633:toxicity*
D002210:Caprylates; D011963:Receptors, GABA-A; D013438:Sulfhydryl Compounds; D000641:Ammonia; C031492:octanoic acid