A longitudinal study of tryptophan involvement in hepatic coma

Hutson, Duane G.; Ono, Jiroichi; Dombro, Roy S.; Levi, Joé U.; Livingstone, Alan S.; Zeppa, Robert

doi:10.1016/0002-9610(79)90153-3

Cited by 28 publications

(8 citation statements)

References 15 publications

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“…Tryptamine metabolism increases with rising tissue tryptophan levels (Warsh et al, 1979;Young et al, 1980 b) and CSF tryptophan is high in patients with liver disease (Young et aI., 1975;Hutson et al, 1979). Therefore, we have looked at CNS tryptamine metabolism in patients with cirrhosis of the liver, by measuring IAA in their lumbar CSF.…”

Section: Introductionmentioning

confidence: 99%

CNS tryptamine metabolism in hepatic coma

Young

Lal

1980

J. Neural Transmission

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Lumbar CSF indoleacetic acid (IAA) was higher in patients with cirrhosis of the liver than in controls. It was also higher in CSF of patients in coma than in those with hepatic cirrhosis but not in coma. There was a strong correlation (r = 0.89, p less than 0.01) between the grade of hepatic coma and CSF IAA. These data indicate that there is an association between elevated CNS tryptamine metabolism and hepatic coma. How far changes in the metabolism of tryptamine and other trace amines are relevant to the induction of hepatic coma or are simply a reflection of advanced liver dysfunction is unclear.

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Section: Introductionmentioning

confidence: 99%

CNS tryptamine metabolism in hepatic coma

Young

Lal

1980

J. Neural Transmission

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“…Ultrafiltration of plasma in Amicon membrane cones with control of pH was successful and convenient for obtaining the free tryptophan fraction^ and this method in combination with HPLC was better for determination Of free tryptophan than any method reported already (16,(18)(19)(20). In this work we examined the effect of pH of plasma d ring centrifugation on the free tryptophan concentration of the filtrate.…”

Section: Discussionmentioning

confidence: 98%

“…Hutson et al (20) reported that after recovery from coma plasma free tryptophan decreased but tryptop han in the CSF remained unchanged. The decrease of plasma free tryptophan may be the result of iniprovement of liver function, and this improvement may decrease the concentrations of substances that evoke coma to values below those effective in producing coma.…”

Section: Discussionmentioning

confidence: 99%

“…In previous reports, the plasma tryptophan is assayed without separating the tryptophan (16,(18)(19)(20), so that contaminants in the sample influence .the value for the tryptophan concentration. Therefore, f rther application of high performance liquid chromatography (HPLC) is useful for the specific determination of tryptophan in the plasma.…”

Section: Introductionmentioning

confidence: 99%

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Determination of Free Tryptophan in Plasma and Its Clinical Applications

Hijikata¹,

Hara²,

Shiozaki³

et al. 1984

Clinical Chemistry and Laboratory Medicine

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Summary: Free tryptophan in plasma was separated by centrifugation through an Amicon Ultrafiltration membrane cone. The value obtained without control of pH was found to be lower than that obtained with control of pH by an improved method (Hijikata et al. (1981) Anal. Biochem. 118, 10-16).For determination of the total tryptophan concentration in the plasma, high performance liquid chromatography (HPLC) was better than the method of Denckla Dewey s modified by Bloxam & Warren ((1974) Anal. Biochem. 60,[621][622][623][624][625], s judged on the basis of sensitivity, recovery rate and coefficient of variance. The total tryptophan concentration in the plasma determined by HPLC was lower than that determined by theThe total tryptophan concentration (t-Trp), free tryptophan concentration (f-Trp) and f-Trp/t-Trp ratio were 55.8 ± 10.2 μιηοΐ/ΐ, 11.6 ± 1.5 μίηοΐ/ΐ and 0.211 ± 0.03 (mean ± l SD) respectively, in healthy subjects (co trols). No significant difference was observed between the values of controls and those of patients with liver cirrhosis, hepatocellular carcinoma, liver cirrhosis with hepatocellular carcinoma and hepatic encephalopathy of liver cirrhosis without bleeding. But in liver cirrhosis with bleeding, free tryptophan concentration (f-Trp, 48.0 ± 23.3 μτηοΐ/ΐ, p < 0.001) and f-Trp/t-Trp ratio (0.645 ± 0.289, p < 0.001) were significantly higher than those of controls. In fulminant hepatitis free tryptophan concentration, (f-Trp, 106.6 ± 79.9 μιηοΐ/ΐ, p < 0.02), and f-Trp/t-Trp ratio (0.973 ± 0.017, p < 0.001) were significantly higher than those of controls, and free tryptophan concentration (f-Trp) and f-Trp/t-Trp ratio (p < 0.005) were significantly higher than in liver cirrhosis with bleeding. In other words the increase of free tryptophan concentration in plasma may be related to the bleeding, and in fulminant hepatitis the binding ability of free tryptophan to albumin may decrease. In the examined cases of liver cirrhosis, the correlation of the concentration of plasma tryptophan with those of other amino acids and indicators of liver function was changed when hepatocellular carcinoma was also present.

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“…Increased plasma concentrations of several neutral amino acids (NAA), including free tryptophan, and increased brain concentrations of tryptophan, the precursor of serotonin, is a consistent finding. High concentrations in the brain and CSF of 5-hydroxyindoleacetic acid (5-HIAA), the degradation product of serotonin, demonstrated in man [3,16,25] and in experimental animals [14,18] with liver failure, may indicate an increased production of brain serotonin.…”

Section: Introductionmentioning

confidence: 99%

The effect of liver ischaemia on brain monoamine synthesis in the rat

et al. 1987

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Subtotal or total liver ischaemia was induced in the rat by dividing the hepatic artery (Expt. I) or by total dearterialisation of the liver (Expt. II) 2 days after porta-caval shunt (PCS). The animals received i.v. a 10% glucose infusion for 5 h after the last operation and were killed by decapitation. At the end of the experiment all animals with liver ischaemia were in Grade III coma. In different regions of the CNS 5-hydroxytryptophan (5-HTP), 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA), were analysed by HPLC-technique with electrochemical detection, while dihydroxyphenylalanine (DOPA), dopamine (DA) and norepinephrine (NE) were analysed with a radio enzymatic method after blocking the decarboxylation of 5-HTP to 5-HT and DOPA to DA by inhibition of the aromatic amino acid decarboxylase enzyme with m-hydroxybenzylhydrazine (NSD 1015) in order to estimate the synthesis rate of 5-hydroxyindoles and catecholamines. In Expt. I concentrations of 5-HTP in animals with PCS were increased as compared to sham operation. In animals with liver ischaemia, 5-HTP concentrations were increased as compared to sham operation but similar to those in animals with PCS alone. These results suggest that ligation of the hepatic artery for 5 h in PCS animals does not further accelerate the rate of brain indole synthesis. In Expt. II, the 5-HTP concentrations were increased in PCS animals as compared to sham operation. Animals with total liver dearterialisation exhibited decreased 5-HTP levels as compared to PCS, suggesting a decreased brain indole synthesis after severe liver ischaemia. In Expt. II, CNS concentrations of DOPA following PCS were unaltered as compared with sham-operated animals. In animals with total liver dearterialisation, DOPA levels were increased, suggesting an augmented catecholamine synthesis. The NE levels were lower than in PCS and in sham-operated animals.

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A longitudinal study of tryptophan involvement in hepatic coma

Cited by 28 publications

References 15 publications

CNS tryptamine metabolism in hepatic coma

CNS tryptamine metabolism in hepatic coma

Determination of Free Tryptophan in Plasma and Its Clinical Applications

The effect of liver ischaemia on brain monoamine synthesis in the rat

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