TY - JOUR A2 - 里德，盖德J. AU - Eisenhut，迈克尔PY - 2019 DA - 2019年11月6日TI - 证据支持这一假设炎症诱发血管痉挛参与收购感觉神经的发病听力损失SP - 4367240 VL- 2019 AB - 神经性听力损失主要是收购并影响全球大约13种十亿人类。它关系到老化，噪音，感染，耳毒性药物，以及遗传缺陷。重要的是要找出可逆和可预防的原因，以便能够减少这种疾病负担。炎症是通过血管痉挛缺血相关参与大多数的原因和导致组织损伤。血管痉挛是可逆的。本文综述了证据的炎症诱发血管痉挛链接到几种形式收购聋。血管痉挛和感觉神经性听力损失之间的联系是在蛛网膜下腔出血，其涉及血管收缩诱导的细胞因子样白细胞介素-1，内皮素-1和肿瘤坏死因子的释放直接明显的。这些促炎细胞因子，也可响应于感染，自身免疫性疾病，急性和慢性或炎症加重在老化生物体如老年聋或噪音诱导的耳蜗损伤释放。血管痉挛和听力损失的证据也已在细菌性脑膜炎和脑损伤发现。 Resolution of inflammation-induced vasospasm has been associated with improvement of hearing in autoimmune diseases involving overproduction of interleukin-1 from inflammasomes. There is mainly indirect evidence for vasospasm-associated sensorineural hearing loss in most forms of systemic or injury- or infection-induced local vascular inflammation. This opens up avenues in prevention and treatment of vascular and systemic inflammation as well as vasospasm itself as a way to prevent and treat most forms of acquired sensorineural hearing loss. Future research needs to investigate interventions antagonising vasospasm and vasospasm-inducing proinflammatory cytokines and their production in randomised controlled trials of prevention and treatment of acquired sensorineural hearing loss. Prime candidates for interventions are hereby inflammasome inhibitors and vasospasm-reducing drugs like nitric oxide donors, rho-kinase inhibitors, and magnesium which have the potential to reduce sensorineural hearing loss in meningitis, exposure to noise, brain injury, arteriosclerosis, and advanced age-related and autoimmune disease-related inflammation. SN - 1687-9201 UR - https://doi.org/10.1155/2019/4367240 DO - 10.1155/2019/4367240 JF - International Journal of Otolaryngology PB - Hindawi KW - ER -