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Am J Physiol Heart Circ Physiol 282: H1871-H1878, 2002. First published January 17, 2002; doi:10.1152/ajpheart.00976.2001
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Vol. 282, Issue 5, H1871-H1878, May 2002

Increased nonoxidative glycolysis despite continued fatty acid uptake during demand-induced myocardial ischemia

Margaret P. Chandler, Hazel Huang, Tracy A. McElfresh, and William C. Stanley

Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106-4970

During stress, patients with coronary artery disease frequently fail to increase coronary flow and myocardial oxygen consumption (MVO2) in response to a greater demand for oxygen, resulting in "demand-induced" ischemia. We tested the hypothesis that dobutamine infusion with flow restriction stimulates nonoxidative glycolysis without a change in MVO2 or fatty acid uptake. Measurements were made in the anterior wall of anesthetized open-chest swine hearts (n = 7). The left anterior descending (LAD) coronary artery flow was controlled via an extracorporeal perfusion circuit, and substrate uptake and oxidation were measured with radiotracers. Demand-induced ischemia was produced with intravenous dobutamine (15 µg · kg-1 · min-1) and 20% reduction in LAD flow for 20 min. Despite no change in MVO2, there was a switch from lactate uptake (5.9 ± 3.1) to production (74.5 ± 16.3 µmol/min), glycogen depletion (66%), and increased glucose uptake (105%), but no change in anterior wall power or the index of anterior wall energy efficiency. There was no change in the rate of tracer-measured fatty acid uptake; however, exogenous fatty acid oxidation decreased by 71%. Thus demand-induced ischemia stimulated nonoxidative glycolysis and lactate production, but did not effect fatty acid uptake despite a fall in exogenous fatty acid oxidation.

angina; dobutamine; heart; energy metabolism


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