alexa Visual evoked potentials in a rabbit model of hepatic encephalopathy. II. Comparison of hyperammonemic encephalopathy, postictal coma, and coma induced by synergistic neurotoxins.
Molecular Biology

Molecular Biology

Journal of Cell Science & Therapy

Author(s): Pappas SC, Ferenci P, Schafer DF, Jones EA

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Abstract To assess neuronal mechanisms of potential importance in the pathogenesis of hepatic encephalopathy, visual evoked potentials were recorded in rabbits with acute hyperammonemic encephalopathy, postictal coma, and toxin-induced coma resulting from the administration of a combination of subcoma doses of three neurotoxins: ammonia, dimethyldisulfide, and octanoic acid. The patterns of visual evoked potentials in these three syndromes were compared with those of rabbits with hepatic encephalopathy due to galactosamine-induced fulminant hepatic failure. In the absence of seizures, the patterns of visual evoked potentials associated with hyperammonemic encephalopathy and toxin-induced coma were fundamentally different from those associated with any stage of hepatic encephalopathy due to galactosamine-induced fulminant hepatic failure. In contrast, the pattern of visual evoked potentials in early postictal coma induced by four different precipitating factors (including toxin-induced seizures) resembled that of late-stage hepatic encephalopathy due to galactosamine-induced fulminant hepatic failure. These findings suggest that the recording of visual evoked potentials may be of value in experimentally testing hypotheses of the pathogenesis of hepatic encephalopathy due to fulminant hepatic failure. They indicate that acute hyperammonemia is not a satisfactory model of hepatic encephalopathy due to galactosamine-induced fulminant hepatic failure, that the occurrence of seizures may lead to incorrect interpretation of experimental data from models of hepatic encephalopathy, and that the syndromes of hepatic encephalopathy due to galactosamine-induced fulminant hepatic failure and postictal coma may share similar neural mechanisms. Finally, the results of this study do not support the hypothesis that hepatic encephalopathy due to galactosamine-induced fulminant hepatic failure is mediated by the synergistic interaction of ammonia, mercaptans, and fatty acids on the brain.
This article was published in Gastroenterology and referenced in Journal of Cell Science & Therapy

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