Several aspects of the myocardial O2 supply/consumption relationship were determined after coronary artery occlusion and subsequent β-adrenergic blockade in 16 anesthetized open-chest dogs. Small artery and vein O2 saturations, and hence extraction, were obtained microspectrophotometrically and combined with radioactive microsphere blood flow determinations to calculate regional myocardial O2 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 O2 saturations, indicating an increased O2 extraction. Ischemic O2 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 O2 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 O2 saturations within the ischemic region decreased dramatically. Venous O2 saturations were elevated relative to the control group resulting in a reduced O2 extraction. The decrease in heterogeneity of arterial and venous O2 saturations suggest that propranolol eliminates microregions of relatively high O2 extraction, consumption, and/or a majority of vessels with extremely low flow. This leads to a significant improvement in the O2 supply/consumption ratio in the ischemic myocardium of the dog. This may be due to a reduction in the heterogeneity and level of β1-adrenergic receptor activity within the heart.
Robert S. Conway, Harvey R. Weiss
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