自19世纪末Habermann发表噪声性聋的耳蜗病理变化以来,至今对噪声损伤机制尚无满意的解释。过去的研究由于各家采用不同的动物标本、噪声暴露方式及检查时间不同等,因此难以对其结果作比较。噪声外伤初起为机械性损害耳蜗结构及其成份的完整性,以后由于外伤使Corti淋巴(Cortilymph,即第三淋巴)和内淋巴的屏障破坏,扰乱了内环境的稳定,耳蜗离子(特别钾、钠离子)浓度改变导致敏感的上皮坏死,坏死程度和范围决定于愈合和坏死过程的平衡,受很多因素影响,不少因素尚不为人所知,但作者们发现在外伤后继续接受生理强度的较低声音刺激可 Since the late 19th century, Habermann published noise-induced deaf pathological changes in the cochlear, so far there is no satisfactory explanation for the mechanism of noise damage. In the past, it was difficult to compare the results of different types of animal specimens, different ways of noise exposure and different examinations. The beginning of the noisy trauma is mechanical damage to the integrity of the cochlear structure and its components. Afterward, the barrier of Cortilymph and endolymphatic vessels is damaged due to trauma, disturbing the stability of the internal environment, cochlear ions (especially potassium , Sodium ion) lead to sensitive epithelial necrosis, the extent and extent of necrosis depends on the balance of the healing and necrosis process, many factors, many factors not yet known, but the authors found that after trauma to continue to receive physiological strength The lower sound stimulation can be