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Analysis of the relationships between cardiac oxygen usage (MVO2), cardiac muscle adenosine levels([Ado]), and coronary vascular resistance (R) in open-chest, anesthetized dogs tested the hypothesis that adenosine is a physiological regulator of coronary flow. Experiments using each dog as its own control showed that [Ado] varied directly with MVO2 as the latter changed spontaneously or in response to atrial pacing, paired pacing, aortic constriction, of beta-adrenergic blockade. In turn, R varied inversely with changes in [Ado]. Stimulating MVO2 with isoproterenol significantly increased the slope of the regression of [Ado] on MVO2 as well as of R-1 on [Ado]. The effect of beta-adrenergic stimulation on [Ado] is unexplained, but its effect on R-1 seems to reflect the combined effects of adenosine and direct beta-adrenergic coronary relaxation. These results support the hypothesis that adenosine mediates the coronary flow responses to changes in MVO2.
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