VISUAL EVOKED-POTENTIALS IN A RABBIT MODEL OF HEPATIC-ENCEPHALOPATHY .2. COMPARISON OF HYPERAMMONEMIC ENCEPHALOPATHY, POSTICTAL COMA, AND COMA INDUCED BY SYNERGISTIC NEUROTOXINS

  • 1 January 1984
    • journal article
    • research article
    • Vol. 86  (3) , 546-551
Abstract
To assess neuronal mechanisms of potential importance in the pathogenesis of hepatic encephalopathy, visual evoked potentials [VEP] 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 3 neurotoxins: ammonia, dimethyldisulfide and octanoic acid. The patterns of VEP in thes 3 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 VEP 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 VEP in early postictal coma induced by 4 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 VEP may be of value in experimentally testing hypotheses of the pathogenesis of hepatic encephalopathy due to fulminant hepatic failure. Acute hyperammonemia apparently is not a satisfactory model of hepatic encephalopathy due to galactosamine-induced fulminant hepatic failure, the occurrence of seizures may lead to incorrect interpretation of experimental data from models of hepatic encephalopathy, and 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.