Sandlin David S, Yu Yue, Huang Jun, Zhang Chunming, Arteaga Alberto A, Lippincott John K, Peeden Erin O H, Guyton Ryan R, Chen Lan, Beneke Laura L S, Allison Jerome C, Zhu Hong, Zhou Wu
Graduate Program in Neuroscience, University of Mississippi Medical Center, Jackson, MS, USA.
School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA.
J Otol. 2018 Jun;13(2):44-53. doi: 10.1016/j.joto.2018.01.001. Epub 2018 Mar 9.
Blast overpressure has become an increasing cause of brain injuries in both military and civilian populations. Though blast's direct effects on the cochlea and vestibular organs are active areas of study, little attention has been given to the ear's contribution to the overall spectrum of blast injury. Acute autonomic responses to blast exposure, including bradycardia and hypotension, can cause hypoxia and contribute to blast-induced neurotrauma. Existing literature suggests that these autonomic responses are elicited through blast impacting the thorax and lungs. We hypothesize that the unprotected ear also provides a vulnerable locus for blast to cause autonomic responses. We designed a blast generator that delivers controlled overpressure waves into the ear canal without impacting surrounding tissues in order to study the ear's specific contribution to blast injury. Anesthetized adult rats' left ears were exposed to a single blast wave ranging from 0 to 110 PSI (0-758 kPa). Blast exposed rats exhibited decreased heart rates and blood pressures with increased blast intensity, similar to results gathered using shock tubes and whole-body exposure in the literature. While rats exposed to blasts below 50 PSI (345 kPa) exhibited increased respiratory rate with increased blast intensity, some rats exposed to blasts higher than 50 PSI (345 kPa) stopped breathing immediately and ultimately died. These autonomic responses were significantly reduced in vagally denervated rats, again similar to whole-body exposure literature. These results support the hypothesis that the unprotected ear contributes to the autonomic responses to blast.
爆炸超压已成为军事和民用人群脑损伤日益增加的一个原因。尽管爆炸对耳蜗和前庭器官的直接影响是研究的活跃领域，但对于耳朵在爆炸伤整体范围中的作用却很少受到关注。对爆炸暴露的急性自主反应，包括心动过缓和低血压，可导致缺氧并促成爆炸诱导的神经创伤。现有文献表明，这些自主反应是通过爆炸冲击胸部和肺部引发的。我们假设，未受保护的耳朵也是爆炸引发自主反应的一个脆弱部位。我们设计了一种爆炸发生器，可将可控的超压波送入耳道而不影响周围组织，以研究耳朵对爆炸伤的具体作用。将麻醉的成年大鼠的左耳暴露于0至110磅力/平方英寸（0至758千帕）的单次爆炸波中。随着爆炸强度增加，暴露于爆炸的大鼠心率和血压降低，这与文献中使用激波管和全身暴露收集的结果相似。虽然暴露于低于50磅力/平方英寸（345千帕）爆炸的大鼠呼吸频率随着爆炸强度增加而增加，但一些暴露于高于50磅力/平方英寸（345千帕）爆炸的大鼠立即停止呼吸并最终死亡。在迷走神经切断的大鼠中，这些自主反应显著降低，这同样与全身暴露文献相似。这些结果支持了未受保护的耳朵促成对爆炸的自主反应这一假设。
