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目的:观察强噪声暴露后大鼠听觉电生理及形态学的改变,为探讨噪声性聋的发病机制提供实验依据。方法:大鼠随机分为对照组和实验组,实验组暴露于中心频率为4kHz的窄带噪声中,给声强度为120 dBSPL,暴露时间为4h。观察2组听觉脑干诱发电位(ABR)及耳蜗形态学的变化。结果:实验组出现ABR反应阈上升,与对照组比较差异有统计学意义(P<0.01);暴露后第1天,基底膜铺片经DNA荧光染料碘化丙锭染色后示:实验组3排外耳毛细胞(OHC)中可出现不同的毛细胞细胞核形态变化(正常、凋亡、坏死和缺失),而第21天未见明显的细胞凋亡;OHC的缺失2组差异有统计学意义(P<0.01),螺旋神经节细胞计数2组差异无统计学意义(P>0.05)。扫描电镜示:实验组OHC纤毛异常(散乱、倒伏)及OHC的缺失,以第3排OHC最严重。结论:所应用的强噪声能引起大鼠听觉系统的损害,产生永久性阈移(PTS)。该噪声条件下,耳蜗毛细胞的死亡模式在暴露后早期包括凋亡和坏死,而晚期则主要是坏死;PTS的产生可能和OHC纤毛异常及OHC的缺失有关。
Objective: To observe the auditory electrophysiological and morphological changes of rat after exposure to strong noise, and to provide experimental basis for exploring the pathogenesis of noise-induced deafness. Methods: The rats were randomly divided into control group and experimental group. The experimental group was exposed to narrowband noise with a center frequency of 4 kHz, giving an intensity of 120 dBSPL and an exposure time of 4 h. The auditory brainstem response (ABR) and cochlear morphological changes in the two groups were observed. Results: The ABR threshold increased in the experimental group compared with the control group (P <0.01). On the first day after exposure, the basement membrane membrane was stained with the DNA fluorescent dye propidium iodide, and the experimental group 3 Different hair cell nuclear morphological changes (normal, apoptotic, necrotic and missing) appeared in the excised ear hair cells (OHC), but no obvious apoptosis was found on the 21th day. There was significant difference between the two groups (P <0.01). There was no significant difference in spiral ganglion cell count between the two groups (P> 0.05). Scanning electron microscopy showed: OHC cilia abnormalities (scattered, lodging) and OHC in the experimental group were the most severe in the third row. Conclusion: The applied strong noise can cause damage to the auditory system of the rat, resulting in a permanent threshold shift (PTS). Under this noise condition, the apoptotic patterns of cochlear hair cells included apoptosis and necrosis in the early post-exposure period, but necrosis in the late stages. The production of PTS may be related to OHC cilia abnormality and OHC loss.