Arterial CO₂, myocardial O₂ consumption, and coronary blood flow in the dog

We determined the effect of changes in arterial PCO₂ on the relationship between O₂ delivery (ḊO₂) and consumption (MV̇O₂) by the myocardium of anesthetized dogs. Left anterior descending coronary blood flow (CVF), arterial and great cardiac vein O₂ content (GCVO₂), and arterial pressure were measured. MV̇O₂ was raised by infusing various doses of isoproterenol (ISO) or norepinephrine (NE) into the right atrium. CBF, ḊO₂, coronary conductance (CVC), and GCVO₂ were plotted as a function of MV̇O₂ using data obtained at high (≃70 mm Hg) and low (≃24 mm Hg) PCO₂. When ISO was used to raise MV̇O₂, we found that CBF, ḊO₂ and CVC were slightly higher for a given MV̇O₂. In addition, GCVO₂ was ≃7 vol % at high CO₂, ≃4 vol % at low CO₂. When NE was used to raise MV̇O₂, this difference was not observed at high MV̇O₂'s. Alpha-receptor blockade caused the results with NE to look more like the results with ISO. Indomethacin lowered GCVO₂ relative to MV̇O₂ under resting conditions at both high and low PCO₂, but not during infusion of ISO. These results indicate that (1) elevation of systemic arterial PCO₂ causes only a small increase ḊO₂ relative to MV̇O₂ but that this results in a relatively large increase in tissue oxygenation, (2) NE causes α receptor-mediated vasoconstriction which competes with CO₂ vasodilation, and (3) prostaglandin release contributes a vasodilator influence at resting but not elevated MV̇O₂.