Effects of repetitive brief ischemia on contractile efficiency and oxygen cost of contractility in dog heart

It is unclear whether preceding repetitive brief ischemia causes any improv ement in the energy efficiency of intracellular calcium cycling or crossbri dge cycling that may lead to cardioprotection after subsequent sustained is chemia/reperfusion, a phenomenon called ischemic preconditioning. To addres s this issue, left ventricular (LV) contractility (E-max) and the relation between myocardial oxygen consumption (VO2) 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 Rep20, 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-ind ependent VO2 recovered to their respective control levels. The oxygen cost of contractility (the slope of the PVA-independent VO2-E-max relation durin g CaCl2 loading) remained constant (Control 0.0019+/-0.0009 vs. Rep-60 0.00 18+/- 0.0013 ml O-2.ml.mmHg(-1).beat(-1).100 g(-2), ns), suggesting unchang ed efficiency in Ca2+ cycling. Also, the contractile efficiency (the recipr ocal of the slope of the VO2-PVA relation, reflecting the efficiency of cro ssbridge cycling) was the same between the Control and Rep-60 (53.7+/-16.7 vs. 55.4+/-14.4%, ns). Basal metabolism VO2 during KCI arrest was also simi lar to that in the normal heart. Nonmechanical energy expenditure was reduc ed in proportion to the decrease in LV contractility after repetitive brief ischemia, while both the contractile efficiency and oxygen cost of contrac tility remained constant. These results indicate that the heart, after repe titive brief ischemia but before sustained ischemia, has normal efficiencie s of crossbridge cycling and Ca2+ cycling despite the transiently reduced c ontractility.