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Visual evoked potentials in encephalopathy induced by galactosamine, ammonia, dimethyldisulfide, and octanoic acid.

Abstract
Visual evoked potentials were utilized to examine the neuronal transmission changes provoked by galactosamine-induced hepatic encephalopathy and by administration in normal animals of toxins presumably involved in the pathogenesis of hepatic encepalopathy. Separate acute administrations of ammonia, dimethyldisulfide, and octanoic acid induced lethargy, convulsions in the case of the first two, and coma with visual-evoked potential patterns that never resembled the evoked potentials recorded in hepatic coma. By contrast, single and repeated administrations of the three above-mentioned toxins together at lower doses induced lethargy and coma with visual-evoked potential patterns similar to those observed in galactosamine-induced hepatic coma. These observations, together with previously published data, are consistent with the concept that the synergistic interaction of these toxins plays a significant role in the pathogenesis of hepatic encephalopathy.
AuthorsM L Zeneroli, E Ventura, M Baraldi, A Penne, E Messori, L Zieve
JournalHepatology (Baltimore, Md.) (Hepatology) 1982 Sep-Oct Vol. 2 Issue 5 Pg. 532-8 ISSN: 0270-9139 [Print] United States
PMID7118066 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Caprylates
  • Disulfides
  • dimethyl disulfide
  • Galactosamine
  • Ammonia
  • octanoic acid
Topics
  • Ammonia (analysis, pharmacology)
  • Animals
  • Brain Chemistry
  • Caprylates (pharmacology)
  • Disulfides (pharmacology)
  • Evoked Potentials, Visual (drug effects)
  • Galactosamine (pharmacology)
  • Hepatic Encephalopathy (physiopathology)
  • Male
  • Rats
  • Rats, Inbred Strains
  • Time Factors

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