Simard J Marc, Pampori Adam, Keledjian Kaspar, Tosun Cigdem, Schwartzbauer Gary, Ivanova Svetlana, Gerzanich Volodymyr
1 Department of Neurosurgery, University of Maryland School of Medicine , Baltimore, Maryland.
J Neurotrauma. 2014 Jul 15;31(14):1292-304. doi: 10.1089/neu.2013.3016. Epub 2014 Jun 3.
Traumatic brain injury (TBI) caused by an explosive blast (blast-TBI) is postulated to result, in part, from transvascular transmission to the brain of a hydrodynamic pulse (a.k.a., volumetric blood surge, ballistic pressure wave, hydrostatic shock, or hydraulic shock) induced in major intrathoracic blood vessels. This mechanism of blast-TBI has not been demonstrated directly. We tested the hypothesis that a blast wave impacting the thorax would induce a hydrodynamic pulse that would cause pathological changes in the brain. We constructed a Thorax-Only Blast Injury Apparatus (TOBIA) and a Jugular-Only Blast Injury Apparatus (JOBIA). TOBIA delivered a collimated blast wave to the right lateral thorax of a rat, precluding direct impact on the cranium. JOBIA delivered a blast wave to the fluid-filled port of an extracorporeal intravenous infusion device whose catheter was inserted retrograde into the jugular vein, precluding lung injury. Long Evans rats were subjected to sublethal injury by TOBIA or JOBIA. Blast injury induced by TOBIA was characterized by apnea and diffuse bilateral hemorrhagic injury to the lungs associated with a transient reduction in pulse oximetry signals. Immunolabeling 24 h after injury by TOBIA showed up-regulation of tumor necrosis factor alpha, ED-1, sulfonylurea receptor 1 (Sur1), and glial fibrillary acidic protein in veins or perivenular tissues and microvessels throughout the brain. The perivenular inflammatory effects induced by TOBIA were prevented by ligating the jugular vein and were reproduced using JOBIA. We conclude that blast injury to the thorax leads to perivenular inflammation, Sur1 up-regulation, and reactive astrocytosis resulting from the induction of a hydrodynamic pulse in the vasculature.
爆炸导致的创伤性脑损伤（blast-TBI）据推测部分是由于胸腔内主要血管中诱发的流体动力脉冲（又称容积性血涌、弹道压力波、流体静压冲击或液压冲击）经血管传导至脑部所致。这种blast-TBI的机制尚未得到直接证实。我们测试了这样一个假设，即冲击胸部的冲击波会诱发流体动力脉冲，进而导致脑部出现病理变化。我们构建了仅作用于胸部的爆炸损伤装置（TOBIA）和仅作用于颈静脉的爆炸损伤装置（JOBIA）。TOBIA向大鼠右侧胸壁发射准直冲击波，避免直接撞击颅骨。JOBIA向体外静脉输液装置充满液体的端口发射冲击波，该装置的导管逆行插入颈静脉，避免肺部损伤。将Long Evans大鼠用TOBIA或JOBIA造成亚致死性损伤。TOBIA诱发的爆炸损伤表现为呼吸暂停以及与脉搏血氧饱和度信号短暂降低相关的双侧肺部弥漫性出血性损伤。TOBIA损伤后24小时的免疫标记显示，整个大脑的静脉、静脉周围组织和微血管中肿瘤坏死因子α、ED-1、磺脲类受体1（Sur1）和胶质纤维酸性蛋白上调。结扎颈静脉可预防TOBIA诱发的静脉周围炎症反应，且JOBIA可重现这种反应。我们得出结论，胸部爆炸损伤会导致静脉周围炎症、Sur1上调以及血管系统中诱发流体动力脉冲所导致的反应性星形细胞增生。
