Proctor Julie L, Xu Su, Guo Sijia, Piskoun Boris, Miller Catriona, Roys Steven, Gullapalli Rao P, Fiskum Gary
Department of Anesthesiology and the Center for Shock Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, MD, USA.
Department of Diagnostic Radiology and Nuclear Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
J Cereb Blood Flow Metab. 2025 May;45(5):945-959. doi: 10.1177/0271678X241299985. Epub 2024 Dec 18.
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.
飞机客舱通常被加压到相当于海拔8000英尺的气压。实验动物在创伤性脑损伤后暴露于与航空医疗后送相关的低压环境中会使神经学预后恶化，而高氧情况会反常地加剧这种恶化。本研究检验了以下假设：大鼠在皮质撞击后暴露于低压环境会减少脑血流量、增加神经炎症并改变脑内神经化学物质。大鼠在创伤后24小时，于常氧或高氧条件下，接受模拟地面（常压）或空中（8000英尺低压）运输。暴露于低压环境导致飞行期间对侧皮质和双侧丘脑的脑血流量降低，且在伤后14天延迟性皮质炎症（ED1免疫反应性）增加。与维持在海平面的大鼠相比，暴露于低压环境的受撞击大鼠皮质肌酸水平更高。暴露于高氧和低压的组合导致飞行期间皮质血流量和总肌酸的最大降幅，且这种情况持续长达两周。总之，暴露于低压环境期间的灌注不足可能导致神经炎症恶化和神经化学失衡。低压期间过量氧气的存在会导致脑血流量长期受到抑制，这表明在低压期间应调整补充氧气量以维持常氧状态。
