| Effect of hyperglycemia and fatty acid oxidation inhibition during aerobic conditions and demand-induced ischemia. | |
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MedLine Citation:
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PMID: 12521928 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Metabolic interventions improve performance during demand-induced ischemia by reducing myocardial lactate production and improving regional systolic function. We tested the hypotheses that 1) stimulation of glycolysis would increase lactate production and improve ventricular wall motion, and 2) the addition of fatty acid oxidation inhibition would reduce lactate production and further improve contractile function. Measurements were made in anesthetized open-chest swine hearts. Three groups, hyperglycemia (HG), HG + oxfenicine (HG + Oxf), and control (CTRL), were treated under aerobic conditions and during demand-induced ischemia. During demand-induced ischemia, HG resulted in greater lactate production and tissue lactate content but had no significant effect on glucose oxidation. HG + Oxf significantly lowered lactate production and increased glucose oxidation compared with both the CTRL and HG groups. Myocardial energy efficiency was greater in the HG and HG + Oxf groups under aerobic conditions but did not change during demand-induced ischemia. Thus enhanced glycolysis resulted in increased energy efficiency under aerobic conditions but significantly enhanced lactate production with no further improvement in function during demand-induced ischemia. Partial inhibition of free fatty acid oxidation in the presence of accelerated glycolysis increased energy efficiency under aerobic conditions and significantly reduced lactate production and enhanced glucose oxidation during demand-induced ischemia. |
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Authors:
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Pedro N Chavez; William C Stanley; Tracy A McElfresh; Hazel Huang; Joseph P Sterk; Margaret P Chandler |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. Date: 2003-01-09 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 284 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2003 May |
Date Detail:
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Created Date: 2003-04-07 Completed Date: 2003-05-15 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1521-7 Citation Subset: IM |
Affiliation:
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Division of Pediatric Pharmacology and Critical Care, Rainbow Babies and Children's Hospital, Cleveland, Ohio 44106, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Coronary Circulation / physiology Disease Models, Animal Fatty Acids, Nonesterified / metabolism* Glycogen / metabolism Glycolysis / physiology Hyperglycemia / metabolism* Lactic Acid / metabolism Myocardial Ischemia / metabolism* Myocardium / metabolism Oxidation-Reduction Physical Conditioning, Animal / physiology* Sus scrofa Ventricular Function, Left / physiology |
| Grant Support | |
ID/Acronym/Agency:
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HL 58653/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Fatty Acids, Nonesterified; 50-21-5/Lactic Acid; 9005-79-2/Glycogen |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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