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Articles in PresS, published online ahead of print January 17, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00976.2001
Submitted on November 7, 2001
Accepted on January 15, 2002
1 Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, USA
* To whom correspondence should be addressed. E-mail: wcs4{at}po.cwru.edu.
During stress, coronary artery disease patients 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 oxidation. 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 i.v. dobutamine (15 µg/kg/min) 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 µmols/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 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 fatty acid oxidation.
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