The brain octopamine and phenylethanolamine content in rats in thioacetamide-induced hepatogenic encephalopathy.

The brain octopamine (OA) and phenylethanolamine (PhEA) content was determined in rats subjected to repeated intraperitoneal administrations of thioacetamide (TAA) known to produce different stages of hepatogenic encephalopathy (HE). A more than 2.5-fold increase of OA and a 2-fold increase of PhEA was observed after prolonged (3 times) administration of TAA, coinciding with impaired ammonia detoxication in brain and with the onset of pathophysiological changes typical for HE. Only insignificant changes in the content of the amines were observed in the early stages of the experiment as well as in the recovery period. The results are consistent with the "false neurotransmitter" hypothesis of Fischer and Baldessarini, assuming the participation of OA and PhEA in the pathogenesis of HE.