The Mechanism of Hearing Loss Due to Acoustic Trauma

声损伤导致听力损失的机制

基本信息

批准号：
63570816
负责人：
NAKAI Yoshiaki
金额：
$ 1.28万
依托单位：
Osaka City University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1988
资助国家：
日本
起止时间：
1988 至 1990
项目状态：
已结题

项目摘要

Blood circulation in the cochlea after exposure to a non-physiological level of sound (100-125 dB SPL, 3h) was investigated by immunohistological methods and blood vessel casting method by SEM. Impaired blood circulation in the capillary of stria vascularis, osseous spiral lamina and spiral prominence, especially strial capillary showed vasoconstriction like change from early time of this sound exposure and its recovery to the normal status needed more than 24 hours. On the other hand, these capillaries showed no remarkable change after relatively physiological sound level (70-80 dB SPL, 20 min) exposure. These data suggest that NITTS (Noise-induced Temporary Threshold Shift) is ascribed to blood circulation impairment in these areas of the cochlea.In the case of endolymphatic hydrops which is the pathological change manifested in the inner ear dysfunction, the acoustic trauma combined, much more damage was recognized in the hair cell in the cochlea. Glycerol administration might slightly decrease this damage.The normal hearing ear was not affected in the shape of evoked Oto Acoustic Emission (e-OAE) by the difference of time duration of 1 K Hz tone burst stimulation. The ear which had endolymphatic hydrops showed lower tone frequency of e-OAE than stimulated frequency. The administration of lidocaine hydrochloride and loop diuretics showed the change of e-OAE curve.Our devised LV therapy was adopted to the treatment of the patients with acoustic trauma and its usefullness was statistically recognized.

通过免疫组织学方法和血管铸造方法，通过SEM研究了接触非物理学水平（100-125 dB SPL，3H）后耳蜗中的血液循环。血管毛细血管，骨螺旋层和螺旋突出（尤其是弦毛细管）的血液循环受损显示出血管收缩，例如从这种声音暴露的早期及其恢复到正常状态的变化，需要超过24小时。另一方面，这些毛细血管在相对生理的声音水平（70-80 dB，20分钟）暴露后没有明显变化。这些数据表明，NITT（噪声引起的暂时阈值移位）归因于耳蜗的这些区域中的血液循环障碍。在内淋巴处理水力局的情况下，这是内耳功能障碍中表现出的病理变化，声音创伤的结合，在头发细胞中识别出更多的损害。甘油给药可能会稍微减少这种损害。正常的听力耳朵不会因1 K Hz音调爆发刺激的时间差异而受到诱发的Oto声发射（E-OAE）的影响。内淋巴水滴的耳朵显示出比刺激频率低的E-OAE音调频率。盐酸利多卡因和循环利尿剂的给药显示了E-OAE曲线的变化。我们设计的LV治疗被用于治疗声学创伤患者，其有用性在统计上被统计地识别出来。