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为探讨自身免疫性感音神经性聋（ASHL）的内耳病理生理学机制，采用听觉电生理技术和酶组织化学方法，观察ASHL模型动物的内耳生理功能与组织内主要酶活性的变化。结果示：听神经复合动作电位和耳蜗徽音器电位阈值明显升高，内淋巴电位（包括负相）幅值均有不同程度的降低，并与血管纹和内淋巴囊局部组织内Na＋－K＋－ATP酶和琥珀酸脱氧酶活性改变之间有相关性。表明自身免疫性内耳损伤，进而造成组织内相关酶代谢异常，是听觉功能障碍的病理基础。
To investigate the pathophysiological mechanism of inner ear of autoimmune sensorineural hearing loss (ASHL), the electrophysiological and enzymatic histochemical methods were used to observe the changes of inner ear physiological function and major enzyme activities in ASHL model animals. The results showed that: the auditory nerve complex action potential and cochlear implant potential threshold increased significantly, the endolymphatic potential (including the negative phase) amplitude decreased to varying degrees, and the vascular pattern and endolymphatic sac local tissue Na + -K + -ATP There was a correlation between changes in enzyme and succinate dehydrogenase activity. Show that autoimmune inner ear injury, and then cause abnormal metabolism of enzymes within the organization, is the pathological basis of auditory dysfunction.