Abstract
It is unclear whether preceding repetitive brief ischemia causes any improvement in the energy efficiency of intracellular calcium cycling or crossbridge cycling that may lead to cardioprotection after subsequent sustained ischemia/reperfusion, a phenomenon called ischemic preconditioning. To address this issue, left ventricular (LV) contractility (Emax) and the relation between myocardial oxygen consumption (V·O2) and pressure-volume area (PVA, a measure of LV total mechanical energy) were assessed before (Control) and 20 min (Rep-20) and 60 min (Rep-60) after repetitive brief ischemia in 11 isolated, blood-perfused dog hearts. At Rep-20, Emax and PVA-independent V·O2 (nonmechanical energy expenditure) decreased by 23.0 ± 19.5 and 13.9 ± 18.0%, respectively (both p < 0.05). However, at Rep-60, both Emax and PVA-independent V·O2 recovered to their respective control levels. The oxygen cost of contractility (the slope of the PVA-independent V·O2-Emax relation during CaCl2 loading) remained constant (Control 0.0019 ± 0.0009 vs. Rep-60 0.0018 ± 0.0013 ml O2·ml·mmHg−1·beat−1·100 g−2, ns), suggesting unchanged efficiency in Ca2+ cycling. Also, the contractile efficiency (the reciprocal of the slope of the V·O2-PVA relation, reflecting the efficiency of crossbridge cycling) was the same between the Control and Rep-60 (53.7 ± 16.7 vs. 55.4 ± 14.4%, ns). Basal metabolism V·O2 during KCl arrest was also similar to that in the normal heart. Nonmechanical energy expenditure was reduced in proportion to the decrease in LV contractility after repetitive brief ischemia, while both the contractile efficiency and oxygen cost of contractility remained constant. These results indicate that the heart, after repetitive brief ischemia but before sustained ischemia, has normal efficiencies of crossbridge cycling and Ca2+ cycling despite the transiently reduced contractility.
