Abstract:—Three weeks after porto‐caval anastomosis, tryptophan and 5‐hydroxyindolylacetic acid concentrations were‐greatly increased in rat brain regions. 5‐Hydroxytryptamine showed smaller increases. Midbrain tyrosine and muscle tyrosine and tryptophan concentrations were also increased. Striatal dopa‐mine concentration was not significantly changed. Unlike previous results from acute liver failure, brain tryptophan changes in this chronic study did not simply reflect plasma‐free tryptophan changes. Midbrain tryptoph… Show more
“…In hepatic failure in animals and man, increased brain [2,4,5,16] and CSF [ 19] lev els of TRP, serotonin and 5-HIAA have been found, suggesting an accelerated serotonin turnover which may contribute to hepatic coma.…”
Section: Discussionmentioning
confidence: 99%
“…High brain levels of tryptophan stimulate se rotonin synthesis in patients dying in hepatic coma [16] and in rats after hepatectomy [14] or portocaval anastomosis [2,4,5].…”
This study was designed to determine regional changes of amino acids and indole amines in the brain and possible interactions between amino acids and indole amines 18 h after hepatectomy in rats. Hepatectomy and glucose infusion alone resulted in a profound increase of most large neutral amino acids (LNAA) in plasma and in the brain except for the branched-chain amino acids (BCAA), which maintained normal or somewhat lower values in plasma. Hepatectomy and infusion of glucose combined with BCAA sharply reduced the plasma and brain amino acid concentrations of other LNAA. Simultaneously the concentrations of serotonin and 5-hydroxyindoleacetic acid were decreased in all brain regions. In both groups of hepatectomized rats there were regional variations of the amino acid and the indole amine concentrations in the brain, but the response to BCAA infusion was generally the same in all brain regions. No difference in survival between the 2 groups could be found.
“…In hepatic failure in animals and man, increased brain [2,4,5,16] and CSF [ 19] lev els of TRP, serotonin and 5-HIAA have been found, suggesting an accelerated serotonin turnover which may contribute to hepatic coma.…”
Section: Discussionmentioning
confidence: 99%
“…High brain levels of tryptophan stimulate se rotonin synthesis in patients dying in hepatic coma [16] and in rats after hepatectomy [14] or portocaval anastomosis [2,4,5].…”
This study was designed to determine regional changes of amino acids and indole amines in the brain and possible interactions between amino acids and indole amines 18 h after hepatectomy in rats. Hepatectomy and glucose infusion alone resulted in a profound increase of most large neutral amino acids (LNAA) in plasma and in the brain except for the branched-chain amino acids (BCAA), which maintained normal or somewhat lower values in plasma. Hepatectomy and infusion of glucose combined with BCAA sharply reduced the plasma and brain amino acid concentrations of other LNAA. Simultaneously the concentrations of serotonin and 5-hydroxyindoleacetic acid were decreased in all brain regions. In both groups of hepatectomized rats there were regional variations of the amino acid and the indole amine concentrations in the brain, but the response to BCAA infusion was generally the same in all brain regions. No difference in survival between the 2 groups could be found.
“…Excessive changes have been found in the central monoamine neurotransmitters in both human and experimental hepatic encephalopathies, and have been attributed, at least in part, to amino acid imbalance in plasma and brain (Fischer et al, 1975Curzon et al, 1975;Fischer and Baldessarini, 1976). In experimental portocaval encephalopathy, there is a diffuse and regional increase in brain tryptophan (Trp), serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) (Knott and Curzon, 1974;Cummings et al, 1976), a decrease in noradrenaline (NA) (Dodsworth et al, 1974), while striatal dopamine (DA) is not significantly changed in these conditions (Curzon et al, 1975).…”
Spectrofluorometric assays of DA, 5-HT and 5-HIAA were performed in different areas of postmortem brains of humans who died in hepatic and uremic coma. Brain DA showed a mild general decrease, the average reduction being 20 to 30 percent of the controls. By contrast, 5-HT and 5-HIAA were markedly increased in most brain areas, most significantly in the reticular and raphé nuclei of the brainstem and in some parts of the limbic system. Despite individual and regional differences, the monoamine changes had similar patterns in both hepatic and uremic coma. These data in human brain which confirm previous clinical and experimental studies in hepatic encephalopathy suggest some common disorders of central monoamine metabolism in endotoxic coma of different origin. Brain edema, a constant feature in toxic coma, is probably due to increased 5-HT content in the brain, the pathophysiologic effect of 5-HT on the blood-brain barrier being well established. The prominent changes of indoleamine metabolism in the reticular brainstem and limbic systems may be related to disorders of consciousness.
“…Furthermore, a group of uninjected rats showed significant positive correlations between free trytophan in plasma and trytophan concentration in brain regions (Curzon, Kantamaneni, Fernando, Woods & Cavanagh, 1975 Another plasma amino acid, tyrosine, did not show similar changes to those of tryptophan. This finding is consistent with the fall of plasma tryptophan being related to its liberation from albumin, as tryptophan is the only amino acid present in plasma in both protein-bound and free states (McMenamy et al, 1957).…”
1Changes of plasma unesterified fatty acid (UFA) and tryptophan concentration in group-housed rats following removal of their cage-mates and the effects of antilipolytic drugs on these changes were investigated. 2 Removal of group-housed 24 h fasted rats but not fed rats from cages resulted in increased plasma UFA concentration in the remaining rats which was associated with significant increases of the proportion of free tryptophan but significant falls of total tryptophan concentration. These rapid changes were not associated with brain tryptophan changes. Plasma tyrosine concentration was unaffected. 3 The fall of plasma tryptophan did not appear to be due to passage into red cells as erythrocyte tryptophan concentration remained unchanged. 4 Plasma UFA concentrations correlated positively and significantly with corticosterone concentrations which were also increased following removal of cage-mates. 5 Plasma UFA increases and tryptophan changes in the fasting rats were both prevented by nicotinic acid or propranolol. Corticosterone concentration was increased by nicotinic acid but unaffected by propranolol. 6 The possible importance of these rapid changes of plasma tryptophan and of their prevention by antilipolytic drugs is discussed.
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