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

Abstract

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.