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采用硫辛酰胺脱氨酶组织化学方法及图象分析技术，研究白噪声暴露后豚鼠耳蜗核一氧化氮合酶（NOS）神经元及NOS活性的变化与听阈的关系，探讨豚鼠耳蜗核NOS神经元在白噪声损伤过程中可能的作用。结果表明，白噪声暴露后耳蜗核NOS阳性神经元的数量及染色强度明显增加，2周达到高峰，3～4周持续高表达，至5周有所恢复，仍高于正常水平。白噪声暴露后7d以内，耳蜗核NOS活性与ABR阈值有分离现象，7d后，NOS活性与ABR阈值呈正相关（r＝0．9571，P＜0．01）。结果提示，白噪声暴露后，耳蜗核NOS可能具有多重作用，NOS活性在一定范围内可能促进损伤修复，过量表达可加重耳蜗神经损伤。
Using lipoamide deaminase histochemical method and image analysis technology to study the cochlear nucleus nitric oxide synthase (NOS) neurons and NOS activity changes in guinea pig cochlea after exposure to white noise and auditory threshold, to investigate the guinea pig cochlear nucleus NOS nerve The possible role of element in white noise damage. The results showed that the number and staining intensity of NOS positive neurons in cochlear nucleus significantly increased after white noise exposure, peaked at 2 weeks, continued to be high at 3 to 4 weeks, recovered to 5 weeks, and still higher than normal. NOS activity in cochlear nucleus was separated from ABR threshold within 7 days after white noise exposure. After 7 days, NOS activity was positively correlated with ABR threshold (r = 0.9571, P <0.01). The results suggest that NOS may play multiple roles in cochlear nucleus after white noise exposure. NOS activity may promote injury repair within a certain range. Overexpression may aggravate cochlear nerve injury.