Proctor Julie L, Mello Kaitlin T, Fang Raymond, Puche Adam C, Rosenthal Robert E, Fourney William L, Leiste Ulrich H, Fiskum Gary
From the Department of Anesthesiology (J.L.P., K.T.M., GF.), University of Maryland School of Medicine, Program in Trauma (R.F., R.E.R.), R. Adams Cowley Shock Trauma Center, University of Maryland Medical Center; U.S. Air Force Center for the Sustainment of Trauma and Readiness Skills (R.F.); Department of Anatomy and Neurobiology (A.C.P.), Department of Emergency Medicine (R.E.R.), University of Maryland School of Medicine, Baltimore; and School of Engineering (W.L.F., U.L.H.), University of Maryland College Park, College Park, Maryland.
J Trauma Acute Care Surg. 2017 Jul;83(1 Suppl 1):S35-S42. doi: 10.1097/TA.0000000000001478.
Occupants of military vehicles targeted by explosive devices often suffer from traumatic brain injury (TBI) and are typically transported by the aeromedical evacuation (AE) system to a military medical center within a few days. This study tested the hypothesis that exposure of rats to AE-relevant hypobaria worsens cerebral axonal injury and neurologic impairment caused by underbody blasts.
Anesthetized adult male rats were secured within cylinders attached to a metal plate, simulating the hull of an armored vehicle. An explosive located under the plate was detonated, resulting in a peak vertical acceleration force on the plate and occupant rats of 100G. Rats remained under normobaria or were exposed to hypobaria equal to 8,000 feet in an altitude chamber for 6 hours, starting at 6 hours to 6 days after blast. At 7 days, rats were tested for vestibulomotor function using the balance beam walking task and euthanized by perfusion. The brains were then analyzed for axonal fiber injury.
The number of internal capsule silver-stained axonal fibers was greater in animals exposed to 100G blast than in shams. Animals exposed to hypobaria starting at 6 hours to 6 days after blast exhibited more silver-stained fibers than those not exposed to hypobaria. Rats exposed to 100% oxygen (O2) during hypobaria at 24 hours postblast displayed greater silver staining and more balance beam foot-faults, in comparison with rats exposed to hypobaria under 21% O2.
Exposure of rats to blast-induced acceleration of 100G increases cerebral axonal injury, which is significantly exacerbated by exposure to hypobaria as early as 6 hours and as late as 6 days postblast. Rats exposed to underbody blasts and then to hypobaria under 100% O2 exhibit increased axonal damage and impaired motor function compared to those subjected to blast and hypobaria under 21% O2. These findings raise concern about the effects of AE-related hypobaria on TBI victims, the timing of AE after TBI, and whether these effects can be mitigated by supplemental oxygen.
乘坐的军车被爆炸装置袭击的人员经常遭受创伤性脑损伤（TBI），通常会在几天内通过空中医疗后送（AE）系统被转运至军事医疗中心。本研究检验了以下假设：使大鼠暴露于与AE相关的低压环境会加重由车底爆炸导致的脑轴突损伤和神经功能障碍。
将麻醉的成年雄性大鼠固定在连接于金属板的圆筒内，模拟装甲车的车体。引爆置于金属板下方的炸药，使得金属板及乘坐大鼠所受的垂直加速度峰值力达到100G。大鼠保持在常压环境下，或在爆炸后6小时至6天内，在海拔舱内暴露于相当于8000英尺高度的低压环境6小时。在第7天，使用平衡木行走任务对大鼠的前庭运动功能进行测试，并通过灌注使其安乐死。然后对大脑进行轴突纤维损伤分析。
遭受100G爆炸的动物，其内囊银染轴突纤维的数量多于假手术组动物。在爆炸后6小时至6天开始暴露于低压环境的动物，其银染纤维比未暴露于低压环境的动物更多。与在21%氧气环境下暴露于低压环境的大鼠相比，在爆炸后24小时低压环境期间暴露于100%氧气（O₂）的大鼠显示出更强的银染以及更多的平衡木行走失误。
使大鼠暴露于100G的爆炸诱导加速度会增加脑轴突损伤，在爆炸后早至6小时、晚至6天暴露于低压环境会显著加剧这种损伤。与在21%氧气环境下遭受爆炸和低压环境的大鼠相比，先遭受车底爆炸然后在100%氧气环境下暴露于低压环境的大鼠表现出轴突损伤增加和运动功能受损。这些发现引发了对与AE相关的低压环境对TBI受害者的影响、TBI后AE的时机以及这些影响是否可通过补充氧气减轻的关注。
