Role of Propranolol in Improvement of the Relationship between O<sub>2</sub> Supply and Consumption in an Ischemic Region of the Dog Heart

Robert S. Conway; Harvey R. Weiss

doi:10.1172/JCI110620

Role of Propranolol in Improvement of the Relationship between O₂ Supply and Consumption in an Ischemic Region of the Dog Heart

Robert S. Conway and Harvey R. Weiss

Published August 1, 1982 - More info

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Abstract

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.