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Departments of 1 Cardiovascular Physiology, 2 Anesthesiology and Resuscitology, and 3 Cardiovascular Medicine, Okayama University Graduate School of Medicine and Dentistry, Okayama, 700-8558; and 4 National Cardiovascular Center Research Institute, Suita, Osaka, 565-8565, Japan
We have found that cardiac temperature proportionally changes O2 cost of contractility, defined as O2 consumption for myocardial total Ca2+ handling normalized to contractility in terms of the end-systolic pressure-volume ratio (maximal elastance, Emax), in the canine left ventricle (temperature sensitivity, Q10 = 2). We have separately found that a decrease in the recirculation fraction (RF) of Ca2+ within myocardial cells underlies an increased O2 cost of Emax in stunned hearts. We therefore hypothesized that a similar change in RF would underlie the Q10 of O2 cost of Emax. We tested this hypothesis by analyzing RF calculated from an exponential decay component of the transiently alternating postextrasystolic potentiation in the canine left ventricle. RF decreased from 0.7 to 0.5 as cardiac temperature increased from 33 to 38°C with Q10 of 0.5, reciprocal to that of O2 cost of Emax. We conclude that Q10 of ATP-consuming reactions involved in Ca2+ handling and Emax response to it could reasonably account for the reciprocal Q10 of RF and O2 cost of Emax.
excitation-contraction coupling; calcium handling; ventricular contractility; sarcoplasmic reticulum
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