Document Detail


Effect of hyperglycemia and fatty acid oxidation inhibition during aerobic conditions and demand-induced ischemia.
MedLine Citation:
PMID:  12521928     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Pedro N Chavez; William C Stanley; Tracy A McElfresh; Hazel Huang; Joseph P Sterk; Margaret P Chandler
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Publication Detail:
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:
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:
Created Date:  2003-04-07     Completed Date:  2003-05-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1521-7     Citation Subset:  IM    
Affiliation:
Division of Pediatric Pharmacology and Critical Care, Rainbow Babies and Children's Hospital, Cleveland, Ohio 44106, USA.
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MeSH Terms
Descriptor/Qualifier:
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:
HL 58653/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
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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