Department of Anesthesiology and the Center for Shock, Trauma and Anesthesiology (STAR) Research, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Department of Diagnostic Radiology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
J Neurotrauma. 2022 Oct;39(19-20):1442-1452. doi: 10.1089/neu.2022.0102. Epub 2022 Jun 14.
Aeromedical evacuation-relevant hypobaria after traumatic brain injury (TBI) leads to increased neurological injury and death in rats relative to those maintained under normobaria. Applicability of rodent brain injury research to humans may be limited, however, by differences in neuroanatomy. Therefore, we developed a model in which ferrets are exposed to polytrauma consisting of controlled cortical impact TBI and hemorrhagic shock subjected 24 h later to 6 h of hypobaria or normobaria. Our objective was to determine whether the deleterious effects of hypobaria observed in rats, with lissencephalic brains, are also present in a species with a human-like gyrencephalic brain. While no deaths were observed, magnetic resonance spectroscopy (MRS) results obtained two days post-injury indicated reduced cortical creatine, -acetylaspartate, gamma-aminobutyric acid, myo-inositol, and glutamate that were not affected by hypobaria. T-weighted magnetic resonance imaging quantification revealed increased hyperintensity volume representing cortical edema at the site of impact after polytrauma. Hypobaria did not exacerbate this focal edema but did lead to overall reductions in total cortical volume. Both normobaric and hypobaric ferrets exhibited impaired spatial memory six days post-injury on the Object Location Test, but no differences were noted between groups. Finally, cortical lesion volume was not exacerbated by hypobaria exposure on day 7 post-injury. Results suggest that air travel 24 h after polytrauma is associated with structural changes in the ferret brain. Future studies should investigate secondary injury from hypobaria after polytrauma in greater detail including alternative outcome measures, time points, and exposure to multiple flights.
创伤性脑损伤 (TBI) 后与航空医疗后送相关的低气压会导致大鼠的神经损伤和死亡率增加，相对于维持在正常气压下的大鼠。然而，由于神经解剖学的差异，啮齿动物脑损伤研究对人类的适用性可能有限。因此，我们开发了一种模型，其中雪貂暴露于多创伤，包括受控皮质撞击 TBI 和随后 24 小时发生的出血性休克，然后在 6 小时的低气压或正常气压下。我们的目的是确定在具有脑裂脑的大鼠中观察到的低气压的有害影响是否也存在于具有人类脑回脑的物种中。虽然没有观察到死亡，但在损伤后两天获得的磁共振波谱 (MRS) 结果表明皮质肌酸、乙酰天门冬氨酸、γ-氨基丁酸、肌醇和谷氨酸减少，而低气压没有影响。T 加权磁共振成像定量显示，多创伤后皮质撞击部位的皮质水肿体积增加。低气压不会使这种局灶性水肿恶化，但确实导致总皮质体积总体减少。在多创伤后 6 天的物体位置测试中，无论是正常气压还是低气压的雪貂，空间记忆都受损，但两组之间没有差异。最后，在损伤后 7 天，低气压暴露并未使皮质病变体积恶化。结果表明，多创伤后 24 小时的航空旅行与雪貂大脑的结构变化有关。未来的研究应更详细地研究多创伤后低气压引起的继发性损伤，包括替代终点、时间点和多次飞行暴露。
