Influence of CO₂ on cardiovascular response to hypoxia in conscious dogs

The modulating effect of CO₂ on the circulatory response to hypoxia in chronically instrumented conscious dogs was examined over a wide range of arterial partial pressure of O₂ [Pa(O₂) (from 80 to 25 Torr)] during a 41-min rebreathing period at three CO₂ levels: hypocapnia (from Pa(CO₂) of 32 to 18 Torr), eucapnia (32 Torr), and mild hypercapnia (40 Torr). Eucapnic and hypercapnic hypoxic responses were also measured after sinoaortic denervation (SAD) to assess the arterial chemoreceptor and baroreceptor reflex contributions. Elevating Pa(CO₂) attenuated the tachycardia during hypoxia and produced progressively greater systemic, renal, and splanchnic vasoconstriction before but not after SAD. Vagal block converted the rises in renal and splanchnic flows observed during hypocapnic hypoxia to declines. The increase in left ventricular dP/dt(max) was not affected by varying Pa(CO₂) either before or after SAD. Coronary flow increased in additional onefold during hypoxia when Pa(CO₂) was elevated both before and after SAD, but the tension-time indices did not differ significantly. These results indicate that: a) cardiopulmonary vagal afferents effectively counteract chemoreflex-induced vasoconstriction during hypocapnic hypoxia; b) chemoreflex vasoconstriction predominantes in the renal and splanchnic beds when Pa(CO₂) is elevated; c) the sinoaortic reflexes restrain the heart rate, but not the contractility response to hypoxia when Pa(CO₂) is increased; and d) the augmented coronary vasodilation produced by CO₂ is probably mediated by local CO₂-hypoxic interactions.