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

以豚鼠为实验对象，探讨了噪声性听力损伤的机制和促进因素。得到的结果如下：1。在120 dB的4kHz纯音环境中连续暴露10分钟后，动物的CAP阈值在暴露后立即升高60 dB，然后在7天后恢复到30 dB的永久性阈值偏移。电诱发耳声发射（eeoae）在暴露后和暴露后7天没有显示任何变化。结果表明，噪声引起的暂时性和永久性阈值移位可能与外毛细胞的机电转导功能障碍有关。糖皮质激素（GR）受体拮抗剂RU38463分别于4 kHz纯音120 dB声压下暴露10分钟后的第0、3和7天给药。与暴露后7天每年注射生理盐水的动物相比，这些动物在5至8 kHz频率下的CAP阈值升高明显严重。2 .耳蜗GR-GR受体系统的下调影响了噪声诱导的临时阈值筛选的恢复，从而加速了对声过度刺激的敏感性。在103db声压级的8khz波段噪声下暴露30分钟前后，测量了12khz eeoae的低频调声。eeoae本身的输出不受暴露的影响，但声调制的幅度下降了50%。人们认为，由于暴露在嘈杂的声音中，MET功能的丧失会降低eeoae中声学调制的幅度。

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.