Rubio Jose E, Skotak Maciej, Alay Eren, Sundaramurthy Aravind, Subramaniam Dhananjay Radhakrishnan, Kote Vivek Bhaskar, Yeoh Stewart, Monson Kenneth, Chandra Namas, Unnikrishnan Ginu, Reifman Jaques
Department of Defense Biotechnology High Performance Computing Software Applications Institute, Telemedicine and Advanced Technology Research Center, United States Army Medical Research and Development Command, Fort Detrick, MD, United States.
The Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., Bethesda, MD, United States.
Front Bioeng Biotechnol. 2020 Dec 17;8:573647. doi: 10.3389/fbioe.2020.573647. eCollection 2020.
The interaction of explosion-induced blast waves with the torso is suspected to contribute to brain injury. In this indirect mechanism, the wave-torso interaction is assumed to generate a blood surge, which ultimately reaches and damages the brain. However, this hypothesis has not been comprehensively and systematically investigated, and the potential role, if any, of the indirect mechanism in causing brain injury remains unclear. In this interdisciplinary study, we performed experiments and developed mathematical models to address this knowledge gap. First, we conducted blast-wave exposures of Sprague-Dawley rats in a shock tube at incident overpressures of 70 and 130 kPa, where we measured carotid-artery and brain pressures while limiting exposure to the torso. Then, we developed three-dimensional (3-D) fluid-structure interaction (FSI) models of the neck and cerebral vasculature and, using the measured carotid-artery pressures, performed simulations to predict mass flow rates and wall shear stresses in the cerebral vasculature. Finally, we developed a 3-D finite element (FE) model of the brain and used the FSI-computed vasculature pressures to drive the FE model to quantify the blast-exposure effects in the brain tissue. The measurements from the torso-only exposure experiments revealed marginal increases in the peak carotid-artery overpressures (from 13.1 to 28.9 kPa). Yet, relative to the blast-free, normotensive condition, the FSI simulations for the blast exposures predicted increases in the peak mass flow rate of up to 255% at the base of the brain and increases in the wall shear stress of up to 289% on the cerebral vasculature. In contrast, our simulations suggest that the effect of the indirect mechanism on the brain-tissue-strain response is negligible (<1%). In summary, our analyses show that the indirect mechanism causes a sudden and abundant stream of blood to rapidly propagate from the torso through the neck to the cerebral vasculature. This blood surge causes a considerable increase in the wall shear stresses in the brain vasculature network, which may lead to functional and structural effects on the cerebral veins and arteries, ultimately leading to vascular pathology. In contrast, our findings do not support the notion of strain-induced brain-tissue damage due to the indirect mechanism.
爆炸产生的冲击波与躯干的相互作用被认为是导致脑损伤的原因之一。在这种间接机制中，冲击波与躯干的相互作用被假定会引发血液涌动，最终到达并损伤大脑。然而，这一假说尚未得到全面系统的研究，间接机制在导致脑损伤方面的潜在作用（如果有的话）仍不明确。在这项跨学科研究中，我们进行了实验并建立了数学模型来填补这一知识空白。首先，我们在冲击管中对斯普拉格-道利大鼠进行了冲击波暴露实验，入射超压分别为70 kPa和130 kPa，在此过程中我们测量了颈动脉和脑部压力，同时将暴露限制在躯干部位。然后，我们建立了颈部和脑血管系统的三维（3-D）流固耦合（FSI）模型，并利用测量到的颈动脉压力进行模拟，以预测脑血管系统中的质量流率和壁面剪应力。最后，我们建立了大脑的三维有限元（FE）模型，并使用FSI计算得到的血管压力来驱动FE模型，以量化冲击波暴露对脑组织的影响。仅对躯干进行暴露实验的测量结果显示，颈动脉峰值超压略有增加（从13.1 kPa增至28.9 kPa）。然而，相对于无冲击波、血压正常的状态，冲击波暴露的FSI模拟预测，在脑底部峰值质量流率增加高达255%，脑血管壁面剪应力增加高达289%。相比之下，我们的模拟结果表明，间接机制对脑组织应变响应的影响可以忽略不计（<1%）。总之，我们的分析表明，间接机制会导致一股突然且大量的血液从躯干迅速通过颈部传播到脑血管系统。这种血液涌动会导致脑血管网络中的壁面剪应力大幅增加，这可能会对脑静脉和动脉产生功能和结构上的影响，最终导致血管病变。相比之下，我们的研究结果不支持间接机制导致应变诱导的脑组织损伤这一观点。
