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Departments of 1 Physiology II, 2 Internal Medicine II, 3 Cardiovascular Medicine, and 4 Anesthesiology and Resuscitology, Okayama University Medical School, Okayama 700-8558; and 5 Department of Anesthesiology and Resuscitology, Faculty of Medicine, Kagoshima University, Kagoshima 890-8520, Japan
Postischemic myocardial stunning halved left ventricular contractility [end-systolic maximum elastance (Emax)] and doubled the O2 cost of Emax in excised cross-circulated canine heart. We hypothesized that this increased O2 cost derived from energy-wasteful myocardial Ca2+ handling consisting of a decreased internal Ca2+ recirculation, some futile Ca2+ cycling, and a depressed Ca2+ reactivity of Emax. We first calculated the internal Ca2+ recirculation fraction (RF) from the exponential decay component of postextrasystolic potentiation. Stunning significantly accelerated the decay and decreased RF from 0.63 to 0.43 on average. We then combined the decreased RF with the halved Emax and its doubled O2 cost and analyzed total Ca2+ handling using our recently developed integrative method. We found a decreased total Ca2+ transport and a considerable shift of the relation between futile Ca2+ cycling and Ca2+ reactivity in an energy-wasteful direction in the stunned heart. These changes in total Ca2+ handling reasonably account for the doubled O2 cost of Emax in stunning, supporting the hypothesis.
stunning; end-systolic maximum elastance; mechanoenergetics; postextrasystolic potentiation
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