Aeromedical evacuation-relevant hypobaria following traumatic brain injury in rats contributes to cerebral blood flow depression, altered neurochemistry and increased neuroinflammation.

Aircraft cabins are routinely pressurized to the equivalent of 8000 ft altitude. Exposure of lab animals to aeromedical evacuation relevant hypobaria after traumatic brain injury worsens neurological outcomes, which is paradoxically exacerbated by hyperoxia. This study tested the hypothesis that exposure of rats to hypobaria following cortical impact reduces cerebral blood flow, increases neuroinflammation, and alters brain neurochemistry. Rats were exposed to simulated ground (normobaric) or air (hypobaric 8000 ft) transport, under normoxia or hyperoxia, 24 hr after trauma. Hypobaria exposure resulted in lower cerebral blood flow to the contralateral cortex and bilateral thalamus during flight and increased delayed cortical inflammation (ED1 immunoreactivity) at 14 days post injury. Impacted rats exposed to hypobaria had higher cortical creatine levels compared rats maintained at sea level. Exposure to the combination of hyperoxia and hypobaria resulted in the greatest reduction in cortical blood flow and total creatine during flight which persisted up to two weeks. In conclusion, hypoperfusion during hypobaria exposure could contribute to worsening of neuroinflammation and neurochemical imbalances. The presence of excessive O during hypobaria results in long-term suppression of cerebral blood flow, indicating that supplemental O should be titrated during hypobaria to maintain normoxia.