Proctor Julie L, Fourney William L, Leiste Ulrich H, Fiskum Gary
From the Department of Anesthesiology (J.L.P., G.F.), and Shock, Trauma, and Anesthesiology Research Center (STAR) (J.L.P., G.F.), School of Medicine, and Department of Mechanical Engineering (W.L.F., U.H.L.), School of Engineering, and the Center of Energetics Concepts Development (W.L.F., U.H.L.), University of Maryland, Baltimore, Maryland.
J Trauma Acute Care Surg. 2014 Sep;77(3 Suppl 2):S83-7. doi: 10.1097/TA.0000000000000340.
More than 300,000 US war fighters in Operations Iraqi and Enduring Freedom have sustained some form of traumatic brain injury (TBI), caused primarily by exposure to blasts. Many victims are occupants in vehicles that are targets of improvised explosive devices. These underbody blasts expose the occupants to vertical acceleration that can range from several to more than 1,000 G; however, it is unknown if blast-induced acceleration alone, in the absence of exposure to blast waves and in the absence of secondary impacts, can cause even mild TBI.
We approached this knowledge gap using rats secured to a metal platform that is accelerated vertically at either 20 G or 50 G in response to detonation of a small explosive (pentaerythritol tetranitrate) located at precise underbody standoff distances. All rats survived the blasts and were perfusion fixed for brain histology at 4 hours to 30 days later.
Robust silver staining indicative of axonal injury was apparent throughout the internal capsule, corpus callosum, and cerebellum within 24 hours after blast exposure and was sustained for at least 7 days. Astrocyte activation, as measured morphologically with brains immunostained for glial fibrillary acidic protein, was also apparent early after the blast and persisted for at least 30 days.
Exposure of rats to underbody blast-induced accelerations at either 20 G or 50 G results in histopathologic evidence of diffuse axonal injury and astrocyte activation but no significant neuronal death. The significance of these results is that they demonstrate that blast-induced vertical acceleration alone, in the absence of exposure to significant blast pressures, causes mild TBI. This unique animal model of TBI caused by underbody blasts may therefore be useful in understanding the pathophysiology of blast-induced mild TBI and for testing medical and engineering-based approaches toward mitigation.
在伊拉克行动和持久自由行动中，超过30万美国战士遭受了某种形式的创伤性脑损伤（TBI），主要是由爆炸暴露所致。许多受害者是简易爆炸装置袭击目标车辆中的乘客。这些车底爆炸使乘客暴露于垂直加速度之下，其范围可达几G至超过1000G；然而，在没有暴露于爆炸波且没有二次撞击的情况下，仅爆炸引起的加速度是否会导致哪怕是轻度的TBI尚不清楚。
我们通过将大鼠固定在金属平台上来填补这一知识空白，该平台会因位于精确车底间隔距离处的小型炸药（季戊四醇四硝酸酯）爆炸而垂直加速至20G或50G。所有大鼠在爆炸中存活，并在4小时至30天后进行灌注固定以进行脑组织学检查。
爆炸暴露后24小时内，在内囊、胼胝体和小脑中可见强烈的银染，表明存在轴突损伤，且这种损伤持续至少7天。用针对胶质纤维酸性蛋白进行免疫染色的大脑进行形态学测量，发现星形胶质细胞激活在爆炸后早期也很明显，并持续至少30天。
将大鼠暴露于20G或50G的车底爆炸诱导加速度下，会导致弥漫性轴突损伤和星形胶质细胞激活的组织病理学证据，但无明显神经元死亡。这些结果的意义在于，它们表明在没有暴露于显著爆炸压力的情况下，仅爆炸诱导的垂直加速度就会导致轻度TBI。因此，这种由车底爆炸引起的TBI独特动物模型可能有助于理解爆炸诱导轻度TBI的病理生理学，并用于测试基于医学和工程的缓解方法。
