EFFECT OF CORONARY HYPEREMIA ON EMAX AND OXYGEN-CONSUMPTION IN BLOOD-PERFUSED RABBIT HEARTS - ENERGETIC CONSEQUENCES OF GREGGS PHENOMENON

To assess the relation between increases in contractile function and oxygen consumption (VO2) during increased coronary flow (Gregg's phenomenon), we measured the end-systolic pressure-volume relation and the relation between VO2 and left ventricular systolic pressure-volume area (PVA, a measure of total mechanical energy output) in blood-perfused, isovolumically contracting rabbit hearts during control and intracoronary adenosine infusion. During adenosine infusion at a constant perfusion pressure (93 +/- 11 mm Hg), coronary flow increased by 99 +/- 76% (p < 0.01), and the slope of the end-systolic pressure-volume relation, E(max) (ventricular contractility index), increased by 18 +/- 15% (p < 0.01). When compared at the same left ventricular volume, PVA increased by 20 +/- 14% (p < 0.01) and VO2 by 19 +/- 15% (p < 0.01) with adenosine. The VO2-PVA relation was linear under each condition (both median r = 0.98). With increased coronary flow, the VO2-intercept of the VO2-PVA relation (unloaded VO2) increased by 22 +/- 18% (p < 0.01) without a change in the slope; that is, a parallel upward shift was observed, indicating that the contractile efficiency (energy conversion efficiency of the contractile machinery) remained constant. These increases in E(max) and unloaded VO2 were not eliminated by beta-adrenergic blockade with propranolol. We conclude that increased coronary flow with adenosine at a constant perfusion pressure augments both E(max) and the nonmechanical energetic cost for excitation-contraction coupling and basal metabolism via nonadrenergic mechanisms, without changing contractile efficiency.