Interaction of hypoxia and hypercapnia on cerebral hemodynamics and brain electrical activity in dogs

Abstract

The interaction of hypoxic hypoxia, hypercapnia, and mean arterial blood pressure (MABP) was studied in 15 pentobarbital-anesthetized ventilated dogs. In one group of animals (n = 5) hypercapnia [arterial CO2 partial pressure (PaCO2) approximately 50 Torr] was added to both moderate hypoxia and severe hypoxia. Moderate hypoxia [arterial O2 partial pressure (PaO2) = 36 mmHg] increased MABP and cerebral blood flow (CBF) without changes in cerebral O2 uptake (CMRO2). Superimposed hypercapnia increased CBF and MABP further with no change in CMRO2. In another group of animals (n = 5), a MABP increase of approximately 40 mmHg during moderate hypoxia without hypercapnia did not further increase CBF, suggesting intact autoregulation. Thus, during moderate hypoxia, hypercapnia is capable of increasing CBF. Severe hypoxia (PaO2 = 22 mmHg) increased CBF, but MABP and CMRO2 declined. Superimposed hypercapnia further decreased MABP and decreased CBF from its elevated level and further decreased CMRO2. Raising MABP under these circumstances in another animal group (n = 5) increased CBF above the level present during severe hypoxia alone and increased CMRO2. The change in CBF and CMRO2 during severe hypoxia plus hypercapnia with MABP elevation were not different from that severe hypoxia alone. We conclude that, during hypoxia sufficiently severe to impair CMRO2, superimposed hypercapnia has a detrimental influence due to decreased MABP, which causes a decrease in CBF and cerebral O2 delivery.