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Experimental Studies on the Mechanism and Promoter of Acoustic Hearing Impairment.

声性听力障碍发生机制及促进因素的实验研究。

基本信息

批准号：
11671718
负责人：
YOSHIDA Masafumi
金额：
$ 1.47万
依托单位：
University of Occupational and Environmental Health
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2001
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671718/
关键词：
Acoustic hearing impairment Outer hair cells Glucocorticoid receptor antagonist Elector-motility Electrically-evoked otoacoustic emissions Modulation by low frequency tones 耳音響放射機械-電気変換 NI-TTS NI-PTS

项目摘要

The mechanism and promoter of noise-induced hearing impairment have been investigated in the animal study using guinea pigs. Obtained results were as follows :1. The CAP thresholds of the animals exposed to 4kHz pure tone at 120 dB for 10 minutes elevated by 60 dB right after the exposure, and then recovered to reach the permanent threshold shift of 30 dB at 7 days after. The electrically evoked otoacoustic emissions (EEOAEs) did not reveal any alteration at the period both right after and 7 days after the exposure. From these result it was concluded that dysfunction of the mechano-electrical transduction (MET) of the outer hair cells was responsible for the noise-induced temporary as well as permanent threshold shift.2. Glucocorticoid (GR) receptor antagonist, RU38463, was administered to the animals at 0, 3 and 7 days after the exposure to 4 kHz pure tone at 120 dB SPL for 10 minutes. The CAP threshold elevation in these animals were significantly sever at the frequencies from 5 to 8 kHz as compared to the saline injected annuals at 7 days after the exposure. Down regulation of GR-GR receptor system in the cochlea affected the recovery fiom noise-induced temporary threshold sift, and thus accelerate the susceptibility to acoustic overstimulation.3. Acoustic modulations of 12 kHz EEOAEs by low frequency tone were measured before and after the exposure to 8 kHz band noise at 103 dB SPL for 30 minutes. The output of the EEOAEs itself was not affected by the exposure, but the magnitudes of acoustic modulation were decreased by 50 %. Loss of the MET function due to loud sound exposure was considered to reduce the magnitude of acoustic modulation in EEOAEs.

本实验采用豚鼠作为实验动物，研究了噪声性听力损伤的机制和促进因素。获得的主要结果如下：1. 4kHz、120 dB纯音暴露10 min后，CAP阈即刻升高60 dB，7 d后恢复至永久性阈移30 dB。电诱发耳声发射（EEOAEs）在暴露后即刻和暴露后7天均无明显变化。结论：外毛细胞的力电转换功能障碍是噪声引起暂时性和永久性阈移的重要原因.在4kHz、120 dBSPL纯音暴露10分钟后0、3、7天分别给予糖皮质激素（GR）受体拮抗剂RU 38463。在暴露后7天，这些动物的CAP阈值在5至8 kHz的频率下显著升高，与注射盐水的一年生动物相比。耳蜗GR-GR受体系统的下调影响了噪声引起的暂时性阈值下降的恢复，从而加速了对声过度刺激的易感性.在暴露于103 dBSPL的8 kHz频带噪声30分钟前后，测量低频纯音对12 kHz EEOAE的声调制。EEOAE本身的输出不受暴露的影响，但声调制的幅度下降了50%。认为由于暴露于高声导致MET功能丧失可降低EEOAE中的声调制幅度。