Department of Biomedical Engineering, University of Minnesota, Twin Cities, 312 Church St. SE, 7-105 Hasselmo Hall, Minneapolis, MN, 55455, USA.
Transl Stroke Res. 2014 Jun;5(3):385-93. doi: 10.1007/s12975-013-0300-3. Epub 2013 Nov 7.
Due to increased survival rates among soldiers exposed to explosive blasts, blast-induced traumatic brain injury (bTBI) has become much more prevalent in recent years. Cerebral vasospasm (CVS) is a common manifestation of brain injury whose incidence is significantly increased in bTBI. CVS is characterized by initial vascular smooth muscle cell (VSMC) hypercontractility, followed by prolonged vessel remodeling and lumen occlusion, and is traditionally associated with subarachnoid hemorrhage (SAH), but recent results suggest that mechanical injury during bTBI can cause mechanotransduced VSMC hypercontractility and phenotype switching necessary for CVS development, even in the absence of SAH. Here, we review the mechanisms by which mechanical stimulation and SAH can synergistically drive CVS progression, complicating treatment options in bTBI patients.
由于接触爆炸冲击的士兵存活率提高,近年来爆炸引起的创伤性脑损伤(bTBI)变得更为普遍。脑血管痉挛(CVS)是脑损伤的一种常见表现,其在 bTBI 中的发生率显著增加。CVS 的特征是初始血管平滑肌细胞(VSMC)过度收缩,随后是血管重塑和管腔闭塞延长,传统上与蛛网膜下腔出血(SAH)相关,但最近的结果表明,bTBI 期间的机械损伤可导致机械转导的 VSMC 过度收缩和 CVS 发展所需的表型转换,即使在没有 SAH 的情况下也是如此。在这里,我们回顾了机械刺激和 SAH 如何协同促进 CVS 进展的机制,这使得 bTBI 患者的治疗选择变得复杂。