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Research Article Free access | 10.1172/JCI113175
Department of Medicine, Los Angeles County Cardiovascular Research Laboratory, UCLA School of Medicine 90024.
Find articles by Marshall, R. in: JCI | PubMed | Google Scholar
Department of Medicine, Los Angeles County Cardiovascular Research Laboratory, UCLA School of Medicine 90024.
Find articles by Nash, W. in: JCI | PubMed | Google Scholar
Department of Medicine, Los Angeles County Cardiovascular Research Laboratory, UCLA School of Medicine 90024.
Find articles by Bersohn, M. in: JCI | PubMed | Google Scholar
Department of Medicine, Los Angeles County Cardiovascular Research Laboratory, UCLA School of Medicine 90024.
Find articles by Wong, G. in: JCI | PubMed | Google Scholar
Published October 1, 1987 - More info
The effect on myocardial energy balance of increasing oxygen demand without altering basal myocardial perfusion rate was assessed in isolated, isovolumic, retrograde blood perfused rabbit hearts. Myocardial energy requirements were increased with paired stimulation. The capacity of rapid paired stimulation to increase mechanical energy consumption was demonstrated in the presence of increased perfusion with the rate X pressure product and oxygen consumption increasing 86 and 148%, respectively, compared with control values. In contrast, rapid paired stimulation under constant, basal flow conditions did not alter the rate X pressure product, while oxygen extraction and consumption increased only 40% relative to control. Myocardial ATP, creatine-phosphate, and lactate content were identical under control and constant flow-paired stimulation conditions. The results of this study indicate that no detectable energy imbalance was produced by rapid paired stimulation with flow held constant at basal rates. These results suggest that the myocardium does not increase mechanical energy expenditure in response to inotropic or rate stimulation in the presence of restricted flow reserve and are inconsistent with the concept of "demand-induced" or "relative" myocardial ischemia.