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目的观察低气压噪声暴露后不同时间豚鼠耳蜗内毛细胞(IHCs)谷氨酸免疫反应(Glu-IR)及听阈的变化。方法按照暴露条件的不同分为四组:低压噪声组、低压组、噪声组和正常对照组。其中,低压噪声组又根据暴露后不同时间点随机分为5小组,即出舱后即刻、8h、1d、3d、7d组,每组动物9只;其余三组各设受试动物9只。豚鼠分组暴露于5500m低气压环境,120dB声压级(SPL)白噪声持续刺激8h。观察暴露后不同时间各组听性脑干反应(ABR)阈的改变,耳蜗IHCs中Glu-IR阳性产物的光密度值。结果低压噪声组和噪声组出舱后8h组ABR阈移最大,与对照组相比有统计学差异(P<0.01),此后两组ABR阈移逐渐恢复,但仍较对照组显著升高(P<0.01)。低压组仅在出舱后即刻出现暂时阈移,此后迅速恢复。低压噪声组出舱即刻IHCs中Glu-IR阳性产物光密度值明显高于对照组(P<0.01),出舱后8h其IHCs内Glu-IR产物光密度值较对照组降低且有统计学差异(P<0.01),出舱后1d、3d和7d组与对照组间无统计学差异。结论低气压可协同噪声环境导致听觉损伤。低气压噪声暴露后,耳蜗IHCs内Glu-IR经过一个增强-减弱-恢复的动态变化过程。低气压噪声环境所致听力损伤可能与IHCs内Glu的变化有关。
Objective To observe the changes of glutamate immune response (Glu-IR) and auditory threshold in guinea pig cochlear inner hair cells (IHCs) at different time after low-noise exposure. The method was divided into four groups according to different exposure conditions: low pressure noise group, low pressure group, noise group and normal control group. Among them, the low-pressure noise group were randomly divided into 5 groups according to different time points after exposure, that is, immediately after the release, 8h, 1d, 3d, 7d group, 9 animals in each group; Guinea pigs were exposed to a low atmospheric pressure of 5500 m and white noise of 120 dB SPL was stimulated for 8 h. The changes of auditory brainstem response (ABR) threshold and the optical density of Glu-IR positive products in cochlear IHCs were observed at different time after exposure. Results Compared with the control group, the threshold of ABR was the highest in the low-noise group and the noise group after 8 h, the difference was statistically significant (P <0.01). After that, the threshold of ABR threshold gradually recovered but remained higher than that of the control group P <0.01). The LV group only had a temporary threshold shift immediately after exiting the cabin and recovered rapidly thereafter. The optical density of Glu-IR positive products in IHCs immediately after exiting of the low-pressure noise group was significantly higher than that of the control group (P <0.01), and the optical density of Glu-IR product in IHCs was significantly lower than that of the control group (P <0.01). There was no significant difference between the control group and the 1st, 3rd, and 7th day after exiting. Conclusions Low pressure can lead to hearing impairment in coordination with noise environment. After exposure to low atmospheric noise, Glu-IR in cochlear IHCs undergoes a dynamic process of enhancement-attenuation-recovery. Hearing impairment caused by low-pressure noise environment may be related to the change of Glu in IHCs.