Liu Tien-Chen, Hsu Chuan-Jen, Hwang Juen-Haur, Tseng Fen-Yu, Chen Yuh-Shyang
Department of Otolaryngology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, ROC.
ORL J Otorhinolaryngol Relat Spec. 2004;66(3):124-9. doi: 10.1159/000079331.
The purpose of this study was to investigate the effects of concomitant exposure to noise and alcohol on the auditory thresholds. Twenty-four guinea pigs were equally divided into three groups: the acute intoxication group, the chronic intoxication group and the control group. Animals in the acute group received single intraperitoneal injections of ethanol (2 g/kg). In the chronic group, alcohol was administered via drinking water (10%, v/v) over a 60-day period. All animals were exposed to a white noise at the intensity of 105 dB A for 30 min. Auditory brainstem response (ABR) thresholds and distortion product otoacoustic emission (DPOAE) levels were measured before, immediately after noise exposure and also 1, 2, and 7 days following exposure. The results showed: first, acute alcohol injection caused a significant, temporary elevation of ABR threshold (4.8 dB in average), while chronic alcohol treatment did not change auditory threshold significantly. Second, noise exposure induced a mean threshold shift of 15.4- 19.7 dB. ABR threshold returned to normal 2 days after exposure. Both acute and chronic alcohol treatment did not alter the magnitude and time course of recovery of the temporary threshold shift (TTS). Third, the mean DPOAE amplitudes decreased at most frequencies following acute injection of alcohol. However, the differences did not reach statistical significance. Fourth, the mean DPOAE levels dropped 3.4-9.6 dB in all groups after noise exposure and returned to normal 1 day to 2 days after noise. There were no significant differences in the amount of DPOAE suppression after noise between the three groups. In summary, we have found that acute and chronic treatment of alcohol in combination with noise did not significantly exacerbate TTS or decrease DPOAE amplitudes relative to noise exposure alone.
本研究的目的是调查噪声与酒精同时暴露对听阈的影响。将24只豚鼠平均分为三组：急性中毒组、慢性中毒组和对照组。急性组动物单次腹腔注射乙醇（2 g/kg）。慢性组动物在60天内通过饮用水给予酒精（10%，v/v）。所有动物均暴露于强度为105 dB A的白噪声中30分钟。在噪声暴露前、暴露后即刻以及暴露后1、2和7天测量听性脑干反应（ABR）阈值和畸变产物耳声发射（DPOAE）水平。结果显示：第一，急性酒精注射导致ABR阈值显著暂时升高（平均4.8 dB），而慢性酒精处理未显著改变听阈。第二，噪声暴露导致平均阈值偏移15.4 - 19.7 dB。ABR阈值在暴露后2天恢复正常。急性和慢性酒精处理均未改变暂时性阈值偏移（TTS）恢复的幅度和时间进程。第三，急性注射酒精后，大多数频率的平均DPOAE幅度降低。然而，差异未达到统计学显著性。第四，噪声暴露后所有组的平均DPOAE水平下降3.4 - 9.6 dB，并在噪声暴露后1至2天恢复正常。三组之间噪声暴露后DPOAE抑制量无显著差异。总之，我们发现相对于单独噪声暴露，急性和慢性酒精处理与噪声联合作用并未显著加重TTS或降低DPOAE幅度。
