The rationale for inotropic support by epinephrine during cardiac surgery and the early postoperative period was examined in 11 dogs after 20 minutes of normothermic ischemia and 1 hour of reperfusion. Ischemia reduced myocardial adenosine 5'-triphosphate (ATP) content by 37%. Left ventricular performance was assessed from pressure-dimension loops generated by minor-axis-diameter crystals for a range of controlled loading as high as end-diastolic pressures of 15 mm Hg. Myocardial oxygen consumption was determined at 6-9 steady-state steps throughout this range, including those at basal conditions of the empty beating ventricle. The hearts were artificially paced at 160 beats/min. Higher oxygen consumption with epinephrine (0.5 microgram/min/kg) administration was demonstrated at all levels of left ventricular performance and at all end-diastolic lengths. Several mechanisms for higher oxygen cost for similar external work performances have been suggested. From this study, it appears that increased uptake of free fatty acids, which increased threefold during epinephrine infusion, contributes to less efficient use of oxygen for mechanical work. We conclude that the use of inotropic support in ischemically injured hearts for reasons other than overt heart failure is not well based because myocardial oxygen consumption increases even when greater work is performed at lower end-diastolic dimensions.