Plasma Amino Acid Imbalance and Hepatic Coma

Munro, H. N.; Wurtman, R. J.

doi:10.1007/978-3-642-66658-2_12

Cited by 34 publications

(27 citation statements)

References 24 publications

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“…It has also been used to explain increased brain tryptophan in liver failure by Munro, Fernstrom & Wurtman (1975) who suggested that plasma insulin elevation in this disorder leads to a fall in the plasma concentrations of branched chain amino acids competing with tryptophan for transport to the brain. Although brain tryptophan changes in various kinds of acute liver failure have been explained largely in terms of plasma free tryptophan changes (Curzon, Knott, Murray-Lyon, Record & Williams, 1975) insulin injection does lead to an increase of brain tryptophan or of the ratio of its concentration to that of plasma free tryptophan (Fernstrom & Wurtman, 1971;Fernando, Knott & Curzon, 1976).…”

Section: Introductionmentioning

confidence: 99%

Effect of Aminophylline on Tryptophan and Other Aromatic Amino Acids in Plasma, Brain and Other Tissues and on Brain 5‐hydroxytryptamine Metabolism

Curzon

Fernando

1976

British J Pharmacology

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1Aminophylline and other methylxanthines increase brain tryptophan and hence 5-hydroxytryptamine turnover. The mechanism of this effect of aminophylline was investigated. 2 At lower doses (t> 100 mg/kg i.p.) the brain tryptophan increase could be explained by the lipolytic action of the drug, i.e. increased plasma unesterified fatty acid freeing plasma tryptophan from protein binding so that it became available to the brain. 3 Plasma unesterified fatty acid did not increase when aminophylline (100 mg/kg i.p.) was given to nicotinamide-treated rats but as both plasma total and free tryptophan rose, a tryptophan increase in the brain still occurred. 4 The rise in brain tryptophan concentration following the injection of a higher dose of the drug (150 mg/kg i.p.) could no longer be explained by a rise of plasma free tryptophan as the ratio of brain tryptophan to plasma free tryptophan rose considerably. Plasma total tryptophan fell and the plasma insulin concentration rose. 5The increase of brain tryptophan concentration after injection of 150 mg/kg aminophylline appeared specific for this amino acid as brain tyrosine and phenylalanine did not increase. However as their plasma concentrations fell the brain/plasma ratio for all three amino acids rose. 6 The higher dose of aminophylline increased the muscle concentration of tryptophan but that of tyrosine fell and that of phenylalanine remained unaltered. The liver concentrations were not affected. 7 The aminophylline-induced increases of the ratio of brain tryptophan to plasma free tryptophan no longer occurred when the drug was given to animals injected with the fl-adrenoceptor blocking agent propranolol or the diabetogenic agent streptozotocin. 8 The changes in brain tryptophan upon aminophylline injection may be explained by (a) increased availability of plasma tryptophan to the brain due to increased lipolysis and (b) increased effectiveness of uptake of tryptophan by the brain due to increased insulin secretion.

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Section: Introductionmentioning

confidence: 99%

Effect of Aminophylline on Tryptophan and Other Aromatic Amino Acids in Plasma, Brain and Other Tissues and on Brain 5‐hydroxytryptamine Metabolism

Curzon

Fernando

1976

British J Pharmacology

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“…There are some studies reporting a relationship between reduction of BCAA and hyperinsulinemia in LC and liver insufficiency (Munro et al 1975;Soeters and Fischer 1976). Hyperinsulinemia, probably caused from deteriorated insulin metabolism in the liver, reduced the blood BCAA levels due to an accelerated consumption in the muscle and the fat tissue (Johnston et al 1977).…”

Section: Dlscusslonmentioning

confidence: 99%

“…However, the contribution of hepatocellular damage and portal-systemic shunting to these changes in plasma amino acid concentrations remained unknown. Decreased plasma levels of BCAA in patients with LC could be ascribed to hyperinsulinemia (Munro et al 1975; Soeters and Fischer 1976). In addition, some invastigators attributed hyperinsulinemia, that is present in LC, to hepatic parenchymal damage (Holdsworth et al 1977;Smith-Laving et al 1979), and others to portal-systemic shunting (Shurberg et al 1977 ; Iwasaki et al 1980).…”

mentioning

confidence: 99%

Plasma amino acid abnormalities in liver disease. Comparative analysis of idiopathic portal hypertension, extrahepatic portal occlusion and liver cirrhosis.

Ouchi

Matsubara

Fukuhara

et al. 1989

Tohoku J. Exp. Med.

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“…Hepatic insufficiency is commonly associated with an increase of plasma aromatic amino acids and a decrease of plasma branched chain amino acids (Fischer 1976). The hyperinsulinemia occurring concomitantly facilitates the decrease in branched chain amino acids, leading to increase in transfer of aromatic amino acids into the brain (Munro et al 1975). Meanwhile, Bloxam and Curzon (1978) reported that brain Trp concentration was more influenced by changes in plasma free Trp concentration than by changes in plasma concentration of competing amino acids.…”

Section: Discussionmentioning

confidence: 99%

Tryptophan metabolism in liver cirrhosis: Influence of oral antibiotics on neuropsychiatric symptoms.

Yoshida

Hirayama

1984

Tohoku J. Exp. Med.

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Oral tryptophan loading tests were performed on patients with cirrhosis of the liver before and after treatment with an oral antibiotic practically unabsorbed from the gastrointestinal tract. After antibiotic therapy, neuropsychiatric manifestations evoked by the oral administration of tryptophan were reduced in duration by about 50% and in severity as well despite a slightly enhanced elevation of serum total and free typtophan levels, compared to pretreatment loading tests, The urinary indican output also showed a significantly greater decrease in the post-treatment test (p <0.05) whereas no appreciable difference was observed in urinary 5-hydroxy-indoleacetic acid excretion between the pre-and post-treatment tests. The data suggest that neuropsychiatric manifestations seen following oral administration of tryptophan may be attributed to intestinal tryptophan metabolites rather than to this aromatic amino acid itself and /or its metabolites in the brain. tryptophan loading ; neuropsychiatric manifestation ; total and free tryptophan ; urinary indican ; urinary 5-hydroxy-indoleacetic acid

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Plasma Amino Acid Imbalance and Hepatic Coma

Cited by 34 publications

References 24 publications

Effect of Aminophylline on Tryptophan and Other Aromatic Amino Acids in Plasma, Brain and Other Tissues and on Brain 5‐hydroxytryptamine Metabolism

Effect of Aminophylline on Tryptophan and Other Aromatic Amino Acids in Plasma, Brain and Other Tissues and on Brain 5‐hydroxytryptamine Metabolism

Plasma amino acid abnormalities in liver disease. Comparative analysis of idiopathic portal hypertension, extrahepatic portal occlusion and liver cirrhosis.

Tryptophan metabolism in liver cirrhosis: Influence of oral antibiotics on neuropsychiatric symptoms.

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