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长期低强度噪声暴露会改变畸变产物耳声发射。

Chronic low-level noise exposure alters distortion product otoacoustic emissions.

作者信息

Skellett R A, Crist J R, Fallon M, Bobbin R P

机构信息

Kresge Hearing Research Laboratory of the South, Department of Otorhinolaryngology and Biocommunication, Louisiana State University Medical Center, New Orleans 70112, USA.

出版信息

Hear Res. 1996 Sep 1;98(1-2):68-76. doi: 10.1016/0378-5955(96)00062-7.

DOI:10.1016/0378-5955(96)00062-7
PMID:8880182
Abstract

Chen et al. (1995) recently reported an altered response to the application of ATP in outer hair cells (OHC) isolated from guinea pigs continuously exposed for 10 or 11 days to a 65 dB SPL (A-scale) narrow-band noise (1.1-2.0 kHz). The primary goal of the present study was to test the hypothesis that the continuous low-level noise used by Chen et al. (1995) alters cochlear function. Cubic (2f1-f2) and quadratic (f2-f1) DPOAEs, as well as, the amount of contralateral suppression of DPOAE amplitudes were chosen for study. Responses were recorded in urethane-anesthetized guinea pigs with sectioned middle ear muscles. The animals had either been exposed to the low-level noise for 3 or 11 days or not exposed at all (n = 13 animals per group). Results demonstrate that this noise induces frequency-dependent and very localized reductions in 2f1-f2 DPOAE input/output (I/O) functions. However, the f2-f1 DPOAE I/O functions appear to be insensitive to the noise exposure. No noise-related changes were found in the amount of contralateral suppression between the different exposure groups, with the exception of one unexplainable data point (f2-f1 DPOAE = 0.5 kHz; day 3) where it was reduced. The 2f1-f2 DPOAE amplitude alterations lend support to the conclusions of Chen et al. (1995) that chronic low-level noise exposure induces molecular changes in the OHCs which may, in turn, alter cochlear function.

摘要

陈等人(1995年)最近报告称,从豚鼠分离出的外毛细胞(OHC)对ATP应用的反应发生了改变,这些豚鼠连续10或11天暴露于65 dB SPL(A计权)窄带噪声(1.1 - 2.0 kHz)中。本研究的主要目的是检验陈等人(1995年)使用的连续低水平噪声会改变耳蜗功能这一假设。选择了三次(2f1 - f2)和二次(f2 - f1)畸变产物耳声发射(DPOAE),以及DPOAE振幅的对侧抑制量进行研究。在中耳肌肉切断的经氨基甲酸乙酯麻醉的豚鼠中记录反应。这些动物要么暴露于低水平噪声3天或11天,要么根本未暴露(每组n = 13只动物)。结果表明,这种噪声会导致2f1 - f2 DPOAE输入/输出(I/O)功能出现频率依赖性且非常局部的降低。然而,f2 - f1 DPOAE的I/O功能似乎对噪声暴露不敏感。除了一个无法解释的数据点(f2 - f1 DPOAE = 0.5 kHz;第3天)其对侧抑制量减少外,不同暴露组之间未发现与噪声相关的对侧抑制量变化。2f1 - f2 DPOAE振幅的改变支持了陈等人(1995年)的结论,即慢性低水平噪声暴露会引起OHC中的分子变化,进而可能改变耳蜗功能。

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