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Conservation of whole body nitric oxide metabolism in human alcoholic liver disease: implications for nitric oxide production.
Scand J Gastroenterol. 2006 Jul; 41(7):820-5.SJ

Abstract

OBJECTIVE

Patients with advanced liver diseases tend to develop a hyperdynamic circulation which complicates cirrhosis. Impairment of nitric oxide (NO) metabolism has been implicated in the pathogenesis of portal hypertension. The aim of this study was to determine nitric oxide synthase (NOS)-dependent whole body NO production in patients with decompensated liver cirrhosis and portal hypertension.

MATERIAL AND METHODS

Ten patients with decompensated alcoholic liver disease and portal hypertension (Child-Pugh Classifications B and C with no signs of infection) and 10 age- and gender-matched control subjects received an intravenous infusion of L-[15N]2-arginine (50 micromol/min for 30 min). Urine and serum nitrite and nitrate concentrations were determined using ion chromatography-mass spectrometry.

RESULTS

NOS-dependent whole body NO synthesis was estimated by the conversion of [15N]guanidino nitrogen of arginine to urine 15N-nitrite and 15N-nitrate. The amount of 15N-nitrite and 15N-nitrate in the urine of patients and control subjects was significantly correlated with the amount of urine nitrite and nitrate over 36 h (r=0.91 and 0.77, respectively, p<0.0001). However, neither a median of 12 h 15N-nitrite and 15N-nitrate nor nitrite and nitrate excretion in the urine was different between patients and control subjects, 46.4 (9.4-152.2) versus 98.7 (29.9-146.5) nmol/mmol creatinine and 20.6 (2.1-69.0) versus 40.0 (27.0-70.1) micromol/mmol creatinine, respectively. No differences were found in serum nitrite and nitrate concentrations and glomerular filtration rates between patients and control subjects, 111.4 (73.2-158.8) versus 109.3 (83.5-176.4) micromol/l.

CONCLUSION

Our results contraindicate a greater basal NOS-dependent whole body NO production in patients with decompensated liver disease and portal hypertension.

Authors+Show Affiliations

Division of Clinical Sciences, University of Sheffield, The Royal Hallamshire Hospital, Sheffield, UK. eric_demoncheaux@yahoo.co.ukNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16785195

Citation

Demoncheaux, Eric A G., et al. "Conservation of Whole Body Nitric Oxide Metabolism in Human Alcoholic Liver Disease: Implications for Nitric Oxide Production." Scandinavian Journal of Gastroenterology, vol. 41, no. 7, 2006, pp. 820-5.
Demoncheaux EA, Elphick DA, Dürner MB, et al. Conservation of whole body nitric oxide metabolism in human alcoholic liver disease: implications for nitric oxide production. Scand J Gastroenterol. 2006;41(7):820-5.
Demoncheaux, E. A., Elphick, D. A., Dürner, M. B., Higgins, G. E., Crowther, D., Williams, E. J., Higenbottam, T. W., & Gleeson, D. (2006). Conservation of whole body nitric oxide metabolism in human alcoholic liver disease: implications for nitric oxide production. Scandinavian Journal of Gastroenterology, 41(7), 820-5.
Demoncheaux EA, et al. Conservation of Whole Body Nitric Oxide Metabolism in Human Alcoholic Liver Disease: Implications for Nitric Oxide Production. Scand J Gastroenterol. 2006;41(7):820-5. PubMed PMID: 16785195.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Conservation of whole body nitric oxide metabolism in human alcoholic liver disease: implications for nitric oxide production. AU - Demoncheaux,Eric A G, AU - Elphick,David A, AU - Dürner,Marc B, AU - Higgins,Gail E, AU - Crowther,David, AU - Williams,Earl J, AU - Higenbottam,Tim W, AU - Gleeson,Dermot, PY - 2006/6/21/pubmed PY - 2006/12/13/medline PY - 2006/6/21/entrez SP - 820 EP - 5 JF - Scandinavian journal of gastroenterology JO - Scand. J. Gastroenterol. VL - 41 IS - 7 N2 - OBJECTIVE: Patients with advanced liver diseases tend to develop a hyperdynamic circulation which complicates cirrhosis. Impairment of nitric oxide (NO) metabolism has been implicated in the pathogenesis of portal hypertension. The aim of this study was to determine nitric oxide synthase (NOS)-dependent whole body NO production in patients with decompensated liver cirrhosis and portal hypertension. MATERIAL AND METHODS: Ten patients with decompensated alcoholic liver disease and portal hypertension (Child-Pugh Classifications B and C with no signs of infection) and 10 age- and gender-matched control subjects received an intravenous infusion of L-[15N]2-arginine (50 micromol/min for 30 min). Urine and serum nitrite and nitrate concentrations were determined using ion chromatography-mass spectrometry. RESULTS: NOS-dependent whole body NO synthesis was estimated by the conversion of [15N]guanidino nitrogen of arginine to urine 15N-nitrite and 15N-nitrate. The amount of 15N-nitrite and 15N-nitrate in the urine of patients and control subjects was significantly correlated with the amount of urine nitrite and nitrate over 36 h (r=0.91 and 0.77, respectively, p<0.0001). However, neither a median of 12 h 15N-nitrite and 15N-nitrate nor nitrite and nitrate excretion in the urine was different between patients and control subjects, 46.4 (9.4-152.2) versus 98.7 (29.9-146.5) nmol/mmol creatinine and 20.6 (2.1-69.0) versus 40.0 (27.0-70.1) micromol/mmol creatinine, respectively. No differences were found in serum nitrite and nitrate concentrations and glomerular filtration rates between patients and control subjects, 111.4 (73.2-158.8) versus 109.3 (83.5-176.4) micromol/l. CONCLUSION: Our results contraindicate a greater basal NOS-dependent whole body NO production in patients with decompensated liver disease and portal hypertension. SN - 0036-5521 UR - https://www.unboundmedicine.com/medline/citation/16785195/Conservation_of_whole_body_nitric_oxide_metabolism_in_human_alcoholic_liver_disease:_implications_for_nitric_oxide_production_ L2 - http://www.tandfonline.com/doi/full/10.1080/00365520500442724 DB - PRIME DP - Unbound Medicine ER -