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 (E(max)) and the relation between myocardial oxygen consumption (VO(2)) 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, E(max) and PVA-independent VO(2) (nonmechanical energy expenditure) decreased by 23.0 +/- 19.5 and 13.9 +/- 18.0%, respectively (both p < 0.05). However, at Rep-60, both E(max) and PVA-independent VO(2) recovered to their respective control levels. The
oxygen cost of contractility (the slope of the PVA-independent VO(2)-E(max) relation during CaCl(2) loading) remained constant (Control 0.0019 +/- 0.0009 vs. Rep-60 0.0018 +/- 0.0013 ml O(2) x ml x mmHg(-1) x beat(-1) x 100 g(-2), ns), suggesting unchanged efficiency in Ca(2+) cycling. Also, the contractile efficiency (the reciprocal of the slope of the VO(2)-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 VO(2) 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 Ca(2+) cycling despite the transiently reduced contractility.