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Am J Physiol Heart Circ Physiol (January 9, 2003). doi:10.1152/ajpheart.00974.2002
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Submitted on November 8, 2002
Accepted on January 3, 2003

Effects of Hyperglycemia and Fatty Acid Oxidation Inhibition during Aerobic Conditions and Demand-induced Ischemia

Pedro N. Chavez1, William C. Stanley2, Tracy A. McElfresh2, Hazel Huang2, Joseph P. Sterk2, and Margaret P. Chandler2*

1 Division of Pediatric Pharmacology and Critical Care, Rainbow Babies and Children's Hospital, Cleveland, OH, USA
2 Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, USA

* To whom correspondence should be addressed. E-mail: mpc10{at}po.cwru.edu.

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); hyperglycemia +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 to 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 FFA 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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