@article{ref1,
title="Does blast exposure to the torso cause a blood surge to the brain?",
journal="Frontiers in bioengineering and biotechnology",
year="2020",
author="Unnikrishnan, Ginu and Chandra, Namas and Monson, Kenneth and Yeoh, Stewart and Kote, Vivek Bhaskar and Reifman, Jaques and Subramaniam, Dhananjay Radhakrishnan and Sundaramurthy, Aravind and Alay, Eren and Skotak, Maciej and Rubio, Jose E.",
volume="8",
number="",
pages="e573647-e573647",
abstract="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.<p /> <p>Language: en</p>",
language="en",
issn="2296-4185",
doi="10.3389/fbioe.2020.573647",
url="http://dx.doi.org/10.3389/fbioe.2020.573647"
}