The effect of halo thane on net myocardial oxygen balance of ischemic myocardium was studied m the non-failing canine heart. Myocardial ischemia was produced by repeated reversible occlusions of a coronary artery; the severity of ischemia was estimated by summating ST-segment elevations (ΣST) obtained by epicardial ECG mapping at 15 to 18 sites. Control measurements were obtained before and after administration of halothane (0.75 percent) to six dogs with chloralose—urethane basal anesthesia. Halothane was associated with significant decreases of systemic arterial pressure (P< .001), heart rate (P< .01), and the product of systolic arterial pressure × heart rate (P< .01), an indirect index of myocardial oxygen consumption, while left atrial pressure remained unchanged at normal levels. ΣST during occlusion was less (P< .001) during halothane (26.5 ± 7.4 {SD} mv) than before (36.G ± 5.4 mv) or after (34.4 ± 8.2 mv) its administration. Thus, halo thane decreased the severity of experimentally-induced myocardial ischemia in the non-failing canine heart. The data suggest that, in the absence of ventricular failure, halothane influences the relationship between myocardial oxygen supply and demand in a favorable direction when coronary blood flow is limited.