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高强度脉冲噪声对豚鼠耳蜗内淋巴中离子浓度的影响。

Effects of high intensity impulse noise on ionic concentrations in cochlear endolymph of the guinea pig.

作者信息

Li W, Zhao L, Jiang S, Gu R

机构信息

Institute of Otolaryngology, Chinese PLA General Hospital, Beijing, China.

出版信息

Chin Med J (Engl). 1997 Nov;110(11):883-6.

PMID:9772424
Abstract

OBJECTIVE

To investigate the effect of acoustic overstimulation on concentrations of cations in cochlear endolymph and analyze the relationship between the ionic changes in endolymph and the hearing loss.

METHODS

The endocochlear potentials (EP), K+, Na+ and Ca2+ concentration in cochlear endolymph were examined in vivo for normal and 167 +/- 2 dB SPL impulse noise exposed groups of guinea pig bored on time course by means of double-barreled ion-selective microelectrodes. Brain stem auditory evoked potential (BAEP) was used to evaluate the auditory function. Ca(2+)-ATPase activity was demonstrated cytochemically in the lateral cochlear wall as induced by Ando et al with slight modification.

RESULTS

The K+ and Ca2+ concentration exhibited significant changes in 8-hour groups (P < 0.05 for K+ and P < 0.01 for Ca2+). Then the K+ concentration was eventually resumed to the initial levels in accordance with the EP recovery in 7 days, while during the same period Ca2+ concentration was always significantly higher than that in control group (P < 0.01). The BAEP threshold shifts were correlated well with changes in ionic concentrations, especially Ca2+ (P < 0.001), in the endolymph induced by acoustic trauma. Although the normal positive EP was observed 7 days after noise exposure, the function of the vascular stria was not completely restored as revealed by the fact that the Ca(2+)-ATPase was diffused to the apical membrane surface.

CONCLUSIONS

Endolymph compartment intrinsic mechanism for maintaining ionic composition is seriously deteriorated after high impulse noise stimulation. The changes of the unique environment of endolymph may play an important role in the mechanism of sensorineural hearing loss induced by acoustic trauma.

摘要

目的

研究声过度刺激对耳蜗内淋巴中阳离子浓度的影响,并分析内淋巴离子变化与听力损失之间的关系。

方法

采用双管离子选择性微电极,在体内按时程检测正常豚鼠组和暴露于167±2 dB SPL脉冲噪声的豚鼠组耳蜗内淋巴的内耳蜗电位(EP)、K⁺、Na⁺和Ca²⁺浓度。用脑干听觉诱发电位(BAEP)评估听觉功能。参照Ando等人的方法并略作修改,采用细胞化学方法显示耳蜗外侧壁的Ca(2+)-ATP酶活性。

结果

8小时组的K⁺和Ca²⁺浓度出现显著变化(K⁺ P < 0.05,Ca²⁺ P < 0.01)。随后,随着7天内EP的恢复,K⁺浓度最终恢复到初始水平,而在此期间,Ca²⁺浓度始终显著高于对照组(P < 0.01)。BAEP阈值变化与声损伤诱导的内淋巴中离子浓度变化,尤其是Ca²⁺浓度变化(P < 0.001)密切相关。尽管噪声暴露7天后观察到正常的正向EP,但血管纹功能并未完全恢复,这一事实表明Ca(2+)-ATP酶扩散到了顶膜表面。

结论

高脉冲噪声刺激后,内淋巴维持离子成分的内在机制严重受损。内淋巴独特环境的变化可能在声损伤诱导的感音神经性听力损失机制中起重要作用。

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