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 O2delivery (DO2) and consumption (MVO2) 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. MVO2 was raised by infusing various doses of isoproterenol (ISO) or norepi-nephrine (NE) into the right atrium. CBF, DO2, coronary conductance (CVC), and GCVO2 were plotted as a function of MVO2 using data obtained at high (⋍70 mm Hg) and low (⋍24 mm Hg) Pco2. When ISO was used to raise MVO2, we found that CBF, DO2, and CVC were slightly higher for a given MV02. In addition, GCVO2 was ⋍7 vol % at high CO2, ⋍4 vol % at low CO2. When NE was used to raise MVO2, this difference was not observed at high MVO2's. Alpha-receptor blockade caused the results with NE to look more like the results with ISO. Indomethacin lowered GCVO2 relative to MV02 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 in DO2 relative to MVO2 but that this results in a relatively large increase in tissue oxygenation, (2) NE causes a receptor-mediated vasocon-striction which competes with CO2 vasodilation, and (3) prostaglandin release contributes a vasodilator influence at resting but not elevated MVO2. Circ Res 47: 217-225, 1980