Enhanced cerebral perfusion during brief exposures to cyclic intermittent hypoxemia

Abstract

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 (VM C A ) and cerebrovascular conductance increased in a sigmoid fashion with decreases in SaO2 and ScO2. 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 VM C A increased from 54.0 ± 0.5 to 57.2 ± 0.5 cm/s (P = 0.0001) and from 53.9 ± 0.5 to 57.1 ± 0.3 cm/s (P = 0.0001) for the SaO2-VM C A and ScO2-VM C A curves, respectively. Cerebral oxygen extraction increased from prehypoxia 0.22 ± 0.01 to 0.25 ± 0.02 in minute 6 of the first hypoxia bout, and remained elevated between 0.25 ± 0.01 and 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. NEW & NOTEWORTHY Five bouts of 6-min intermittent hypoxia (IH) exposures to 10% O2 progressively reduce arterial oxygen saturation (SaO2) to 67% without causing discomfort or distress. Cerebrovascular responses to hypoxemia are dynamically reset over the course of a single IH session, such that threshold and saturation for cerebral vasodilations occurred at lower SaO2 and cerebral tissue oxygenation (ScO2) during the fifth vs. first hypoxia bouts. Cerebral oxygen extraction is augmented during acute hypoxemia, which compensates for decreased arterial O2 content.