Abstract
Onboard oxygen-generating systems (OBOGSs) provide increased inspired oxygen (F(i)O(2)) to mitigate the risk of neurologic injury in high altitude aviators. OBOGSs can deliver highly variable oxygen concentrations oscillating around a predetermined F(i)O(2) set point, even when the aircraft cabin altitude is relatively stable. Steady-state exposure to 100% F(i)O(2) evokes neurovascular vasoconstriction, diminished cerebral perfusion, and altered electroencephalographic activity. Whether non-steady-state F(i)O(2) exposure leads to similar outcomes is unknown. This study characterized the physiologic responses to steady-state and non-steady-state F(i)O(2) during normobaric and hypobaric environmental pressures emulating cockpit pressures within tactical aircraft. The participants received an indwelling radial arterial catheter while exposed to steady-state or non-steady-state F(i)O(2) levels oscillating ± 15% of prescribed set points in a hypobaric chamber. Steady-state exposure to 21% F(i)O(2) during normobaria produced arterial blood gas values within the anticipated ranges. Exposure to non-steady-state F(i)O(2) led to P(a)O(2) levels higher upon cessation of non-steady-state F(i)O(2) than when measured during steady-state exposure. This pattern was consistent across all F(i)O(2) ranges, at each barometric condition. Prefrontal cortical activation during cognitive testing was lower following exposure to non-steady-state F(i)O(2) >50% and <100% during both normobaria and hypobaria of 494 mmHg. The serum analyte levels (IL-6, IP-10, MCP-1, MDC, IL-15, and VEGF-D) increased 48 h following the exposures. We found non-steady-state F(i)O(2) levels >50% reduced prefrontal cortical brain activation during the cognitive challenge, consistent with an evoked pattern of neurovascular constriction and dilation.