Plasma levels of false neurotransmitters across the brain in portal-systemic encephalopathy

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Abstract
Arterial and internal jugular venous levels of false neurotransmitters (FNT): octopamine, OCT, and phenylethanolamine (PEA), aromatic and branched-chain amino acids, glutamine, ammonia and pH were measured in patients with portal-systemic encephalopathy (PSE) and in appropriate controls to define the role of these parameters in the pathogenesis of hepatic coma. The typical plasma patterns reported in the literature were observed: hyperammonemia (59 .+-. 8 .mu.mol/l vs. controls 30 .+-. 4, P < 0.005), elevated OCT (19 .+-. 3 nmol/l vs. 6 .+-. 1, P < 0.001) and PEA (64 .+-. 8 nmol/l vs. 27 .+-. 3, P < 0.001), high ratio of aromatic to branched-chain amino acids (0.92 .+-. 0.12 vs. 0.32 .+-. 0.04, P < 0.005), and variable glutamine levels (216-734 .mu.mol/l). No consistent net flux into or out of the brain could be demonstrated for any of these substances. The degree of encephalopathy correlated with the level of respiratory alkalosis (r = 0.325, P < 0.05) which, in turn, correlated with the degree of elevation of plasma OCT (r = 0.439, P < 0.05) and PEA (r = 0.489, P < 0.05) and with the excess of glutamine efflux from the brain (r = 0.927, P < 0.05). Hyperammonemia, plasma amino acid imbalance and elevated production of FNT are apparently interrelated disturbances which contribute to the pathogenesis of PSE. Alkalosis accentuates the altered metabolism of these substances within the brain.