CEREBRAL OXYGEN AVAILABILITY BY NIR SPECTROSCOPY DURING TRANSIENT HYPOXIA IN HUMANS

The effects of mild hypoxia on brain oxyhemoglobin, cytochrome a,a3 redox status, and cerebral blood volume were studied using near-infrared spectroscopy in eight healthy volunteers. Incremental hypoxia reaching 70% arterial O2 saturation was produced in normocapnia [end-tidal PCO2 (PET(CO2)) 36.9 ± 2.6 to 34.9 ± 3.4 Torr] or hypocapnia (P(ET(CO2)) 32.8 ± 0.6 to 23.7 ± 0.6 Torr) by an 8-min rebreathing technique and regulation of inspired CO2. Normocapnic hypoxia was characterized by progressive reductions in arterial PO2 (Pa(O2), 89.1 ± 3.5 to 34.1 ± 0.1 Torr) with stable P(ET(CO2)), arterial P(CO2) (Pa(CO2)), and arterial pH and resulted in increases in heart rate (35%) systolic blood pressure (14%), and minute ventilation (5-fold). Hypocapnic hypoxia resulted in progressively decreasing Pa(O2) (100.2 ± 3.6 to 28.9 ± 0.1 Torr), with progressive reduction in Pa(CO2) (39.0 ± 1.6 to 27.3 ± 1.9 Torr), and an increase in arterial pH (7.41 ± 0.02 to 7.53 ± 0.03), heart rate (61%), and ventilation (3-fold). In the brain, hypoxia resulted in a steady decline of cerebral oxyhemoglobin content and a decrease in oxidized cytochrome a,a3. Significantly greater loss of oxidized cytochrome a,a3 occurred for a given decrease in oxyhemoglobin during hypocapnic hypoxia relative to normocapnic hypoxia. Total blood volume response during hypoxia also was significantly attenuated by hypocapnia, because the increase in volume was only half that of normocapnic subjects. We conclude that cytochrome a,a3 oxidation level in vivo decreases at mild levels of hypoxia. Pa(CO2) is an important determinant of brain oxygenation, because it modulates ventilatory, cardiovascular, and cerebral O2 delivery responses to hypoxia.