| Single dose of glutamine enhances myocardial tissue metabolism, glutathione content, and improves myocardial function after ischemia-reperfusion injury. | |
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MedLine Citation:
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PMID: 14621120 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Myocardial ischemia and reperfusion (I/R) injury causes significant morbidity and mortality. Protection against I/R injury may occur via preservation of tissue metabolism and ATP content, preservation of reduced glutathione, and stimulation of heat shock protein (HSP) synthesis. Supplementation with glutamine (GLN) has been reported to have beneficial effects on all of these protective pathways. Thus, we hypothesized that GLN pretreatment given to the rat in vivo would protect the myocardium against I/R-induced dysfunction. METHODS: GLN (0.52 g/kg, intraperitoneally, given as alanine-glutamine dipeptide), alanine alone (0.23 g/kg), or a Ringer's lactate solution (control) was administered to Sprague-Dawley rats 18 hours before heart excision, perfusion, exposure to global ischemia (15 minutes) and reperfusion (1 hour). Tissue metabolites were analyzed via magnetic resonance spectroscopy. RESULTS: In control and alanine-treated animals, I/R injury resulted in cardiac dysfunction, indicated by a decrease in cardiac output. Administration of GLN 18 hours before I/R injury preserved cardiac output after reperfusion. Metabolic analysis of the myocardial tissue revealed that [/R injury led to significant diminution of myocardial tissue glutamate, ATP content, accumulation of myocardial lactate, and a reduction in reduced glutathione content in control animals. GLN significantly reduced the deleterious changes in myocardial metabolism and improved reduced glutathione content. No changes in pre- or post-I/R injury HSP expression were observed after GLN administration. CONCLUSIONS: These observations demonstrate that remote in vivo administration of GLN before cardiac I/R injury can improve post-I/R cardiac function. This effect may be mediated via improved myocardial metabolism and enhanced reduced glutathione content. |
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Authors:
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Paul E Wischmeyer; David Jayakar; Ursula Williams; Kristen D Singleton; Jacob Riehm; Emile A Bacha; Valluvan Jeevanandam; Uwe Christians; Natalie Serkova |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: JPEN. Journal of parenteral and enteral nutrition Volume: 27 ISSN: 0148-6071 ISO Abbreviation: JPEN J Parenter Enteral Nutr Publication Date: 2003 Nov-Dec |
Date Detail:
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Created Date: 2003-11-17 Completed Date: 2004-04-27 Revised Date: 2007-02-21 |
Medline Journal Info:
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Nlm Unique ID: 7804134 Medline TA: JPEN J Parenter Enteral Nutr Country: United States |
Other Details:
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Languages: eng Pagination: 396-403 Citation Subset: IM |
Affiliation:
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Department of Anesthesiology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA. paul.wischmeyer@UCHSC.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Diphosphate
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analysis Adenosine Triphosphate / analysis Alanine / administration & dosage Animals Cardiac Output / drug effects, physiology Coronary Circulation / drug effects, physiology Disease Models, Animal Dose-Response Relationship, Drug Glucose / analysis Glutamine / administration & dosage* Glutathione / drug effects*, metabolism* HSP72 Heat-Shock Proteins Heart / drug effects*, physiology Heart Rate / drug effects, physiology Heat-Shock Proteins / biosynthesis, drug effects Injections, Intravenous Lactic Acid / metabolism Male Models, Cardiovascular Myocardial Reperfusion Injury / metabolism*, physiopathology* Myocardium / chemistry, metabolism* NAD / drug effects, metabolism Rats Rats, Sprague-Dawley Time Factors |
| Chemical | |
Reg. No./Substance:
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0/HSP72 Heat-Shock Proteins; 0/Heat-Shock Proteins; 50-21-5/Lactic Acid; 50-99-7/Glucose; 53-84-9/NAD; 56-41-7/Alanine; 56-65-5/Adenosine Triphosphate; 56-85-9/Glutamine; 58-64-0/Adenosine Diphosphate; 70-18-8/Glutathione |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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