Enhanced cerebral perfusion during brief exposures to cyclic intermittent hypoxemia

Xiaoli Liu, Diqun Xu, James R Hall, Sarah Ross, Shande Chen, Howe Liu, Robert T Mallet, Xiangrong Shi

Cerebral vasodilation and increased cerebral oxygen extraction help maintain cerebral oxygen uptake in the face of hypoxemia. This study examined cerebrovascular responses to intermittent hypoxemia in eight healthy men breathing 10% O2 for 5 cycles, each 6 min, interspersed with 4 min of room air breathing. Hypoxia exposures raised heart rate (P<0.01) without altering arterial pressure, and increased ventilation (P<0.01) by expanding tidal volume. Arterial oxygen saturation (SaO2) and cerebral tissue oxygenation (ScO2) fell (P<0.01) less appreciably in the first bout (from 97.0±0.3% and 72.8±1.6% to 75.5±0.9% and 54.5±0.9%, respectively) than the fifth bout (from 94.9±0.4% and 70.8±1.0% to 66.7±2.3% and 49.2±1.5%, respectively). Flow velocity in the middle cerebral artery (VMCA) and cerebrovascular conductance increased with decreases in SaO2 and ScO2 in a sigmoid fashion. These stimulus-response curves shifted leftward and upward from the first to the fifth hypoxia bouts; thus, the centering points fell from 79.2±1.4 to 74.6±1.1% (P=0.01) and from 59.8±1.0 to 56.6±0.3% (P=0.002), and the minimum VMCA increased from 54.0±0.5 to 57.2±0.5 cm•s(-1) (P=0.0001) and from 53.9±0.5 to 57.1±0.3 cm•s(-1) (P=0.0001) for the SaO2-VMCA and ScO2-VMCA curves, respectively. Cerebral oxygen extraction increased from pre-hypoxia 0.22±0.01 to 0.25±0.02 in minute 6 of the first hypoxia bout, and remained elevated at 0.25±0.01 - 0.27±0.01 throughout the fifth hypoxia bout. These results demonstrate that cerebral vasodilation combined with enhanced cerebral oxygen extraction fully compensated for decreased oxygen content during acute, cyclic hypoxemia.