Vascular and inflammatory factors in the pathophysiology of blast-induced brain injury.
Vascular and inflammatory factors in the pathophysiology of blast-induced brain injury.
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DOI：
10.3389/fneur.2015.00048
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发表时间：
2015
影响因子：
3.4
通讯作者：
Ahlers ST
中科院分区：
文献类型：
--
作者：
Elder GA;Gama Sosa MA;De Gasperi R;Stone JR;Dickstein DL;Haghighi F;Hof PR;Ahlers ST
爆炸相关创伤性脑损伤（TBI）由于其在伊拉克和阿富汗冲突中的频繁发生而受到广泛关注。这种新的兴趣导致了与爆炸有关的临床和动物研究的迅速扩展。在人类中，高水平爆炸暴露与显著的出血成分有关。在动物模型中，冲击波对神经系统产生各种影响，包括血管和炎症效应，即使是低水平的冲击波暴露也可以看到这些影响，这些影响产生最小或没有神经元病变。急性冲击波暴露可引起动物明显的血管痉挛和脑血流量沿着减少，同时伴有血脑屏障破坏和血管通透性增加。除了对中枢神经系统的直接影响外，有证据支持爆炸的胸腔介导效应的作用;通过体循环传播的压力波损害大脑。长期以来，已观察到与血管细胞外基质改变相关的血管病理学。持续的小胶质细胞和星形胶质细胞反应发生后爆炸曝光。中枢和外周炎症反应的标志物在冲击伤后持续存在，包括炎性细胞因子和其他炎性介质的升高。在低水平的冲击波暴露下，在存在其他正常脑实质的情况下观察到微血管病理学，表明血管系统可能选择性地易受冲击波损伤。在没有直接神经元病理学的情况下，血管损伤后脑中的慢性免疫激活可能导致神经行为改变。旨在预防或逆转血管损伤或调节免疫反应的策略可能会改善与爆炸相关的TBI相关的慢性神经精神症状。
Blast-related traumatic brain injury (TBI) has received much recent attention because of its frequency in the conflicts in Iraq and Afghanistan. This renewed interest has led to a rapid expansion of clinical and animal studies related to blast. In humans, high-level blast exposure is associated with a prominent hemorrhagic component. In animal models, blast exerts a variety of effects on the nervous system including vascular and inflammatory effects that can be seen with even low-level blast exposures which produce minimal or no neuronal pathology. Acutely, blast exposure in animals causes prominent vasospasm and decreased cerebral blood flow along with blood-brain barrier breakdown and increased vascular permeability. Besides direct effects on the central nervous system, evidence supports a role for a thoracically mediated effect of blast; whereby, pressure waves transmitted through the systemic circulation damage the brain. Chronically, a vascular pathology has been observed that is associated with alterations of the vascular extracellular matrix. Sustained microglial and astroglial reactions occur after blast exposure. Markers of a central and peripheral inflammatory response are found for sustained periods after blast injury and include elevation of inflammatory cytokines and other inflammatory mediators. At low levels of blast exposure, a microvascular pathology has been observed in the presence of an otherwise normal brain parenchyma, suggesting that the vasculature may be selectively vulnerable to blast injury. Chronic immune activation in brain following vascular injury may lead to neurobehavioral changes in the absence of direct neuronal pathology. Strategies aimed at preventing or reversing vascular damage or modulating the immune response may improve the chronic neuropsychiatric symptoms associated with blast-related TBI.
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影响因子：
3.4
作者：
Ahlers ST;Vasserman-Stokes E;Shaughness MC;Hall AA;Shear DA;Chavko M;McCarron RM;Stone JR
通讯作者：
Stone JR
影响因子：
3.8
作者：
Bolander, Richard;Mathie, Blake;Vandevord, Pamela
通讯作者：
Vandevord, Pamela
影响因子：
2.5
作者：
Arun, Peethambaran;Abu-Taleb, Rania;Nambiar, Madhusoodana P.
通讯作者：
Nambiar, Madhusoodana P.
影响因子：
2.3
作者：
Adams, Sherry;Condrey, Jillian A.;Davenport, Paul W.
通讯作者：
Davenport, Paul W.
影响因子：
4.8
作者：
Armonda, Rocco A.;Bell, Randy S.;Campbell, William W.
通讯作者：
Campbell, William W.