Several aspects of the myocardial O(2) supply/consumption relationship were determined after coronary artery occlusion and subsequent beta-adrenergic blockade in 16 anesthetized open-chest dogs. Small artery and vein O(2) saturations, and hence extraction, were obtained microspectrophotometrically and combined with radioactive microsphere blood flow determinations to calculate regional myocardial O(2) consumption. Eight dogs remained untreated after coronary artery ligation while another group was given 2 mg/kg propranolol, 10 min after occlusion. Untreated occlusion resulted in decreased arterial and especially venous O(2) saturations, indicating an increased O(2) extraction. Ischemic O(2) consumption was reduced and the subendocardial/subepicardial consumption ratio was reversed (1.26 vs. 0.37) due to the pattern of occluded area flow. Calculated O(2) supply/consumption also decreased. Propranolol produced no significant changes in volume or distribution of flow within the ischemic region while reducing flow, extraction, and consumption in the unoccluded region. The heterogeneity of arterial and particularly venous O(2) saturations within the ischemic region decreased dramatically. Venous O(2) saturations were elevated relative to the control group resulting in a reduced O(2) extraction. The decrease in heterogeneity of arterial and venous O(2) saturations suggest that propranolol eliminates microregions of relatively high O(2) extraction, consumption, and/or a majority of vessels with extremely low flow. This leads to a significant improvement in the O(2) supply/consumption ratio in the ischemic myocardium of the dog. This may be due to a reduction in the heterogeneity and level of beta(1)-adrenergic receptor activity within the heart.