目的 :探讨一氧化氮 ( NO)在噪声性聋发病中的作用。方法 :用中高频连续稳态噪声制作噪声性聋的动物模型 ,用 NADPH-黄递酶组织化学、原位杂交和 Northern印迹法 ,观察噪声刺激对耳蜗一氧化氮合酶 ( NOS)表达的影响。结果 :组织化学法显示 NOS主要分布于内外毛细胞、螺旋神经节细胞和血管纹边缘细胞 ;原位杂交法发现 NOSm RNA在内外毛细胞、螺旋神经节细胞胞浆内均可见阳性染色 ,但血管纹边缘细胞无阳性染色 ;Northern印迹法显示实验组 NOSm RNA表达较对照组增强。结论 :听觉传入径路上存在 Glu:NMDA受体 ,NO:c GMP通路 ,噪声刺激诱发的 NO合成具有介导神经中毒作用 ,血管纹边缘细胞能合成一定量 NO,对耳蜗微循环具有调节作用 Objective: To investigate the role of nitric oxide (NO) in the pathogenesis of noise-induced deafness. Methods: Animal model of noise-induced deafness was made by medium and high frequency continuous steady-state noise. The effects of noise stimulation on the expression of nitric oxide synthase (NOS) in the cochlea were observed by NADPH-diaphorase histochemistry, in situ hybridization and Northern blotting . Results: Histochemical staining showed that NOS mainly distributed in the inner and outer hair cells, spiral ganglion cells and marginal cells of the stria vascularis. In situ hybridization revealed positive staining of NOSm RNA in the cytoplasm of both inner and outer hair cells and spiral ganglion cells. However, There was no positive staining of borderline cells. Northern blotting showed that the expression of NOSmRNA in the experimental group was enhanced compared with the control group. CONCLUSION: There is Glu: NMDA receptor and NO: c GMP pathway on auditory afferent pathways. NOS induced by noise stimulation can mediate neurotoxicity. The marginal cells of stria vascularis can synthesize a certain amount of NO and have a regulation on cochlear microcirculation