Department of Mining and Nuclear Engineering, Missouri University of Science and Technology, Rolla, MO 65401, USA.
Department of Pathology & Anatomical Sciences, University of Missouri School of Medicine, Columbia, MO 65212, USA.
Mil Med. 2021 Jan 25;186(Suppl 1):601-609. doi: 10.1093/milmed/usaa290.
Blast overpressure exposure, an important cause of traumatic brain injury (TBI), may occur during combat or military training. TBI, most commonly mild TBI, is considered a signature injury of recent combat in Iraq and Afghanistan. Low intensity primary blast-induced TBI (bTBI), caused by exposure to an explosive shock wave, commonly leaves no obvious physical external signs. Numerous studies have been conducted to understand its biological effects; however, the role of shock wave energy as related to bTBI remains poorly understood. This report combines shock wave analysis with established biological effects on the mouse brain to provide insights into the effects of shock wave physics as related to low intensity bTBI outcomes from both open-air and shock tube environments.
Shock wave peak pressure, rise time, positive phase duration, impulse, shock velocity, and particle velocity were measured using the Missouri open-air blast model from 16 blast experiments totaling 122 mice to quantify physical shock wave properties. Open-air shock waves were generated by detonating 350-g 1-m suspended Composition C-4 charges with targets on 1-m elevated stands at 2.15, 3, 4, and 7 m from the source.
All mice sustained brain injury with no observable head movement, because of mice experiencing lower dynamic pressures than calculated in shock tubes. Impulse, pressure loading over time, was found to be directly related to bTBI severity and is a primary shock physics variable that relates to bTBI.
The physical blast properties including shock wave peak pressure, rise time, positive phase duration, impulse, shock velocity, and particle velocity were examined using the Missouri open-air blast model in mice with associated neurobehavioral deficits. The blast-exposed mice sustained ultrastructural abnormalities in mitochondria, myelinated axons, and synapses, implicating that primary low intensity blast leads to nanoscale brain damage by providing the link to its pathogenesis. The velocity of the shock wave reflected back from the target stand was calculated from high-speed video and compared with that of the incident shock wave velocity. Peak incident pressure measured from high sample rate sensors was found to be within 1% of the velocity recorded by the high-speed camera, concluding that using sensors in or close to an animal brain can provide useful information regarding shock velocity within the brain, leading to more advanced knowledge between shock wave physics and tissue damage that leads to bTBIs.
爆炸超压暴露是创伤性脑损伤（TBI）的一个重要原因，可能发生在战斗或军事训练期间。TBI 通常是轻度 TBI，被认为是伊拉克和阿富汗近期战斗的标志性损伤。由爆炸冲击波引起的低强度原发性爆炸诱导性 TBI（bTBI），通常没有明显的外部物理迹象。已经进行了许多研究来了解其生物学效应；然而，冲击波能量与 bTBI 的关系仍未得到很好的理解。本报告将冲击波分析与小鼠大脑的已建立的生物学效应相结合，提供了对与开放空气和冲击波管环境中的低强度 bTBI 结果相关的冲击波物理效应的深入了解。
使用来自 16 个爆炸实验的总共 122 只小鼠的密苏里开放空气爆炸模型测量冲击波峰值压力、上升时间、正相持续时间、脉冲、冲击波速度和质点速度，以量化物理冲击波特性。开放空气冲击波是通过引爆 350 克悬挂 C-4 炸药在距离源 2.15、3、4 和 7 米的 1 米高架台上的目标来产生的。
所有小鼠都出现了脑损伤，但没有观察到头的运动，这是因为老鼠经历的动态压力低于冲击波管中的计算值。发现脉冲、随时间施加的压力负载与 bTBI 的严重程度直接相关，是与 bTBI 相关的主要冲击波物理变量。
使用密苏里开放空气爆炸模型检查了包括冲击波峰值压力、上升时间、正相持续时间、脉冲、冲击波速度和质点速度在内的物理爆炸特性，并与相关的神经行为缺陷进行了比较。暴露于爆炸的小鼠的线粒体、髓鞘轴突和突触出现超微结构异常，这表明原发性低强度爆炸通过提供与发病机制的联系，导致纳米级脑损伤。从高速视频计算反射自目标支架的冲击波速度，并与入射冲击波速度进行比较。从高采样率传感器测量到的峰值入射压力与高速摄像机记录的速度相差在 1%以内，这表明在动物大脑内部或附近使用传感器可以提供有关大脑内冲击波速度的有用信息，从而在冲击波物理与导致 bTBI 的组织损伤之间获得更先进的知识。
