[Acute liver damage due to thioacetamide. Morphology, biochemistry and neurophysiologic comparison with cerebrotoxic substances].
Morphology, biochemistry and neurophysiological comparisons with effects of brain-toxic substances. The acute damage of the liver by thioacetamide is characterized neurophysiologically by a far--reached synchronous beginning of cortical and subcortical alteration of activity, a retardation of cortical and subcortical EEG, threshold increase of the EEG--arousal reaction, reductions in amplitude of centrally evoked potentials and increase of acoustically evoked potentials. We impute that according to an acute "toxic" damage of the liver a "membrane hyperpolarisation" results in all or nearly all areas of the brain. A general decrease of excitability of the brain seems consequently plausible. In opposition to this results only activities of the cortex or structures nearby the cortex (areas above the midbrain reticular formation) will be affected by exogenous arterial hyperammoniemia up to 1700 mug/100 ml.
D000081:Acetamides / Q000633:toxicity*; D000085:Acetates / Q000633:toxicity; D000208:Acute Disease; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000503:physiopathology; D001927:Brain Diseases / Q000139:chemically induced*; D002415:Cats; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology*; D004569:Electroencephalography; D006501:Hepatic Encephalopathy / Q000139:chemically induced; D010648:Phenylacetates / Q000097:blood; D000644:Quaternary Ammonium Compounds / Q000097:blood / Q000633:toxicity; D013853:Thioacetamide / Q000633:toxicity*
D000081:Acetamides; D000085:Acetates; D010648:Phenylacetates; D000644:Quaternary Ammonium Compounds; D013853:Thioacetamide
Akute Leberschädigung durch Thioazetamid. Morphologie, Biochemie und neurophysiologische Vergleiche mit Wirkungen hirntoxischer Substanzen