| Effects of L-arginine pretreatment on nitric oxide metabolism and hepatosplanchnic perfusion during porcine endotoxemia. | |
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MedLine Citation:
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PMID: 21508091 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Sepsis is accompanied by an increased need for and a decreased supply of arginine, reflecting a condition of arginine deficiency. OBJECTIVE: The objective was to evaluate the effects of l-arginine pretreatment on arginine-nitric oxide (NO) production and hepatosplanchnic perfusion during subsequent endotoxemia. DESIGN: In a randomized controlled trial, pigs (20-25 kg) received 3 μg . kg(-1) . min(-1) lipopolysaccharide (LPS; 5 endotoxin units/ng) intravenously and saline resuscitation. l-Arginine (n = 8; 5.3 μmol . kg(-1) . min(-1)) or saline (n = 8) was infused starting 12 h before LPS infusion and continued for 24 h after the endotoxin infusion ended. Whole-body appearance rates, portal-drained viscera (PDV), and liver fluxes of arginine, citrulline, NO, and arginine de novo synthesis were measured by using stable-isotope infusion of [(15)N(2)]arginine and [(13)C-(2)H(2)]citrulline. Hepatosplanchnic perfusion was assessed by using a primed continuous infusion of para-aminohippuric acid and jejunal intramucosal partial pressure of carbon dioxide and was related to systemic hemodynamics. RESULTS: Arginine supplementation before LPS increased whole-body NO production in the PDV but not in the liver. Furthermore, it increased blood flow in the portal vein but not in the aorta and hepatic artery. During endotoxin infusion, arginine pretreatment was associated with an increased whole-body arginine appearance and NO production in the gut. Additional effects included a preserved mean arterial pressure, the prevention of an increase in pulmonary arterial pressure, an attenuated metabolic acidosis, and an attenuated increase in the intramucosal partial pressure of carbon dioxide. CONCLUSION: Arginine treatment starting before endotoxemia appears to be beneficial because it improves hepatosplanchnic perfusion and oxygenation during prolonged endotoxemia, probably through an enhancement in NO synthesis, without causing deleterious systemic side effects. |
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Authors:
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Martijn Poeze; Maaike J Bruins; Fons Kessels; Yvette C Luiking; Wouter H Lamers; Nicolaas E P Deutz |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-04-20 |
Journal Detail:
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Title: The American journal of clinical nutrition Volume: 93 ISSN: 1938-3207 ISO Abbreviation: Am. J. Clin. Nutr. Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-05-23 Completed Date: 2011-07-28 Revised Date: 2012-11-22 |
Medline Journal Info:
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Nlm Unique ID: 0376027 Medline TA: Am J Clin Nutr Country: United States |
Other Details:
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Languages: eng Pagination: 1237-47 Citation Subset: AIM; IM |
Affiliation:
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Department of Surgery, Maastricht University Medical Center, Maastricht, Netherlands, Maastricht, Netherlands. m.poeze@ah.unimaas.nl |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acidosis
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prevention & control Animals Arginine / deficiency, pharmacology*, therapeutic use Bacteria / chemistry* Blood Pressure / drug effects Carbon Dioxide / metabolism Dietary Supplements Disease Models, Animal Endotoxemia / blood, drug therapy, metabolism* Female Gastrointestinal Tract / metabolism Lipopolysaccharides Liver / blood supply, drug effects*, metabolism Mucous Membrane / metabolism Nitric Oxide / biosynthesis* Portal Vein / drug effects* Random Allocation Splanchnic Circulation / drug effects*, physiology Swine |
| Grant Support | |
ID/Acronym/Agency:
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R01 GM084447/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Lipopolysaccharides; 10102-43-9/Nitric Oxide; 124-38-9/Carbon Dioxide; 74-79-3/Arginine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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