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用７１只豚鼠，耳后进路暴霜圆窗，置入ＮａＣ１或ＫＣ１或蔗糖晶体，测试不同时间组动物的耳蜗神经动作电位（ＡＰ），并观察内耳的形态学改变。结果：置ＮａＣ１或ＫＣ１后，ＡＰ阈值明显提高，潜伏期延长，但随时间延长，ＡＰ阈值有所下降；病理学研究发现置ＮａＣ１或ＫＣ１后耳蜗损伤仅局限在１、２周，前庭器也有病理学变化；置蔗糖后无上述情况出现。结果提示；圆窗放置ＮａＣ１和ＫＣ１对内耳的损伤可能与Ｎａ＋或Ｋ＋进入内耳产生的化学迷路炎有关，且其损伤属不可逆性改变。
A total of 71 guinea pigs were used in the study. The rats were exposed to round stools and stained with NaC1 or KC1 or sucrose crystals. Cochlear nerve action potential (AP) was measured at different time points and morphological changes of the inner ear were observed. Results: After setting NaC1 or KC1, the AP threshold was significantly increased and the latency was prolonged. However, the AP threshold decreased with time. Pathological studies showed that the damage of cochlear was only limited to 1 and 2 weeks after NaC1 or KC1 implantation. Neo-Confucianism changes; set sucrose after the above situation does not occur. The results suggest that the injury of inner ear caused by NaC1 and KC1 in the round window may be related to the chemical labyrinthitis induced by Na + or K + entering the inner ear, and the damage is irreversible.