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Plasma levels of false neurotransmitters across the brain in portal‐systemic encephalopathy
Author(s) -
CANGIANO CARLO,
FARBER MARK O.,
CARDELLICANGIANO PATRIZIA,
ROSSIFANELLI FILIPPO,
CASCINO ANTONIA,
CAPOCACCIA LIVIO,
COCKERILL EDWARD M.,
MANFREDI FELICE
Publication year - 1982
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1982.tb00934.x
Subject(s) - glutamine , medicine , hepatic encephalopathy , endocrinology , pathogenesis , chemistry , encephalopathy , aromatic amino acids , amino acid , biochemistry , cirrhosis
. Arterial and internal jugular venous levels of false neurotransmitters (FNTs: 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: hyperammonaemia (59 ± 8 μmol/l v. controls 30 ± 4, P < 0.005), elevated OCT (19 ± 3 nmol/l v. 6 ± 1, P < 0.001) and PEA (64 ± 8 nmol/l v. 27 ± 3, P < 0.001), high ratio of aromatic to branched‐chain amino acids (0.92 ± 0.12 v. 0.32 ± 0.04, P < 0.005), and variable glutamine levels (216–734 μmol/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) as well as with the excess of glutamine efflux from the brain ( r = 0.927, P < 0.05). These findings support current views that hyperammonaemia, plasma amino acid imbalance, and elevated production of FNTs are interrelated disturbances which contribute to the pathogenesis of PSE. In addition, the data suggest that alkalosis accentuates the altered metabolism of these substances within the brain.