Splanchnic and peripheral release of 3-methylhistidine in relation to its urinary excretion in human infection

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Standard

Splanchnic and peripheral release of 3-methylhistidine in relation to its urinary excretion in human infection. / Sjölin, J; Stjernström, H; Henneberg, S; Andersson, E; Mårtensson, J; Friman, G; Larsson, J.

I: Metabolism, Bind 38, Nr. 1, 01.01.1989, s. 23-9.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Sjölin, J, Stjernström, H, Henneberg, S, Andersson, E, Mårtensson, J, Friman, G & Larsson, J 1989, 'Splanchnic and peripheral release of 3-methylhistidine in relation to its urinary excretion in human infection', Metabolism, bind 38, nr. 1, s. 23-9.

APA

Sjölin, J., Stjernström, H., Henneberg, S., Andersson, E., Mårtensson, J., Friman, G., & Larsson, J. (1989). Splanchnic and peripheral release of 3-methylhistidine in relation to its urinary excretion in human infection. Metabolism, 38(1), 23-9.

Vancouver

Sjölin J, Stjernström H, Henneberg S, Andersson E, Mårtensson J, Friman G o.a. Splanchnic and peripheral release of 3-methylhistidine in relation to its urinary excretion in human infection. Metabolism. 1989 jan. 1;38(1):23-9.

Author

Sjölin, J ; Stjernström, H ; Henneberg, S ; Andersson, E ; Mårtensson, J ; Friman, G ; Larsson, J. / Splanchnic and peripheral release of 3-methylhistidine in relation to its urinary excretion in human infection. I: Metabolism. 1989 ; Bind 38, Nr. 1. s. 23-9.

Bibtex

@article{7a69d63a5b534c0db4f595c752737ba3,
title = "Splanchnic and peripheral release of 3-methylhistidine in relation to its urinary excretion in human infection",
abstract = "The present investigation was undertaken in order to determine the release of 3-methylhistidine (3MH) from the splanchnic region and from the leg, and the contributions these make to the increase in urinary 3MH excretion in infection. Thirteen febrile patients with infection were investigated. After an overnight fast, hepatic vein, femoral vein, and radial artery catheterizations were performed. Splanchnic and leg blood flows were determined by dye dilution technique. Plasma 3MH was analyzed by a modified HPLC method. The release of 3MH from the leg was 0.064 +/- 0.007 mumol/min (+/- SE) and from the splanchnic region 0.012 +/- 0.013 mumol/min. These releases of 3MH constitute 27% +/- 2% and 8% +/- 6% of the individual urinary excretions, respectively. With increasing degree of catabolism, measured as individual 3MH increase above baseline excretion or as the 3MH to creatinine ratio (3MH:Cr), the relative contribution to urinary excretion from the leg was increased (individual increase, P = 0.08; 3MH:Cr, P less than 0.01). Since this contribution was not decreased in the more catabolic patients, as would have been expected if the increase in urinary 3MH originated elsewhere, it is concluded that skeletal muscle is the source, and these results thus validate the use of urinary 3MH excretion as a marker of myofibrillar protein catabolism in infected patients.",
author = "J Sj{\"o}lin and H Stjernstr{\"o}m and S Henneberg and E Andersson and J M{\aa}rtensson and G Friman and J Larsson",
year = "1989",
month = jan,
day = "1",
language = "English",
volume = "38",
pages = "23--9",
journal = "Metabolism",
issn = "0026-0495",
publisher = "Elsevier",
number = "1",

}

RIS

TY - JOUR

T1 - Splanchnic and peripheral release of 3-methylhistidine in relation to its urinary excretion in human infection

AU - Sjölin, J

AU - Stjernström, H

AU - Henneberg, S

AU - Andersson, E

AU - Mårtensson, J

AU - Friman, G

AU - Larsson, J

PY - 1989/1/1

Y1 - 1989/1/1

N2 - The present investigation was undertaken in order to determine the release of 3-methylhistidine (3MH) from the splanchnic region and from the leg, and the contributions these make to the increase in urinary 3MH excretion in infection. Thirteen febrile patients with infection were investigated. After an overnight fast, hepatic vein, femoral vein, and radial artery catheterizations were performed. Splanchnic and leg blood flows were determined by dye dilution technique. Plasma 3MH was analyzed by a modified HPLC method. The release of 3MH from the leg was 0.064 +/- 0.007 mumol/min (+/- SE) and from the splanchnic region 0.012 +/- 0.013 mumol/min. These releases of 3MH constitute 27% +/- 2% and 8% +/- 6% of the individual urinary excretions, respectively. With increasing degree of catabolism, measured as individual 3MH increase above baseline excretion or as the 3MH to creatinine ratio (3MH:Cr), the relative contribution to urinary excretion from the leg was increased (individual increase, P = 0.08; 3MH:Cr, P less than 0.01). Since this contribution was not decreased in the more catabolic patients, as would have been expected if the increase in urinary 3MH originated elsewhere, it is concluded that skeletal muscle is the source, and these results thus validate the use of urinary 3MH excretion as a marker of myofibrillar protein catabolism in infected patients.

AB - The present investigation was undertaken in order to determine the release of 3-methylhistidine (3MH) from the splanchnic region and from the leg, and the contributions these make to the increase in urinary 3MH excretion in infection. Thirteen febrile patients with infection were investigated. After an overnight fast, hepatic vein, femoral vein, and radial artery catheterizations were performed. Splanchnic and leg blood flows were determined by dye dilution technique. Plasma 3MH was analyzed by a modified HPLC method. The release of 3MH from the leg was 0.064 +/- 0.007 mumol/min (+/- SE) and from the splanchnic region 0.012 +/- 0.013 mumol/min. These releases of 3MH constitute 27% +/- 2% and 8% +/- 6% of the individual urinary excretions, respectively. With increasing degree of catabolism, measured as individual 3MH increase above baseline excretion or as the 3MH to creatinine ratio (3MH:Cr), the relative contribution to urinary excretion from the leg was increased (individual increase, P = 0.08; 3MH:Cr, P less than 0.01). Since this contribution was not decreased in the more catabolic patients, as would have been expected if the increase in urinary 3MH originated elsewhere, it is concluded that skeletal muscle is the source, and these results thus validate the use of urinary 3MH excretion as a marker of myofibrillar protein catabolism in infected patients.

M3 - Journal article

VL - 38

SP - 23

EP - 29

JO - Metabolism

JF - Metabolism

SN - 0026-0495

IS - 1

ER -

ID: 34100148