Ruan Run-Sheng
Department of Otolaryngology, National University of Singapore, Singapore.
Ann N Y Acad Sci. 2002 May;962:260-74. doi: 10.1111/j.1749-6632.2002.tb04073.x.
Nitric oxide (NO) has been implicated as a mediator of vasodilation and neurotransmission in the mammalian cochlea. This is demonstrated by the presence of nitric oxide synthase (NOS) and nitric oxide (NO) in the blood vessels and the organ of Corti in the cochlea. It is not certain if the neurons in the spiral ganglion produce NO since no fluorescent signal could be detected by 4,5-diaminofluorescein diacetate (DAF-2DA), a fluorescent indicator of NO. To determine if NO/peroxynitrite plays any role in neurodestruction observed in ischemic cochlea of the guinea pig, the effects of NO donors, such as S-nitrosocysteine (S-NC) and nitroglycerine (NTG); peroxynitrite generators, such as 3-morpholinosydnonimine (SIN-1); peroxynitrite inhibitors, such as superoxide dismutase plus catalase (SOD/Cat); and NOS inhibitors, such as N(G)-nitro-L-arginine methyl ether (L-NAME) were tested on normal and ischemic cochleae. The level of NO in the cochlea after 20 to 120 minutes of ischemia was indicated by measurement of nitrites/nitrates in the perilymph. The evidence gathered from these experiments indicates that NO or peroxynitrite is not necessarily destructive to auditory hair cells, and in fact, exogenous NO may protect neural structures in the cochlea from damage under ischemic conditions.
一氧化氮（NO）被认为是哺乳动物耳蜗血管舒张和神经传递的介质。耳蜗血管和柯蒂氏器中存在一氧化氮合酶（NOS）和一氧化氮（NO）证明了这一点。由于作为NO荧光指示剂的二乙酸4,5-二氨基荧光素（DAF-2DA）未检测到荧光信号，因此尚不确定螺旋神经节中的神经元是否产生NO。为了确定NO/过氧亚硝酸盐在豚鼠缺血性耳蜗中观察到的神经破坏中是否起任何作用，测试了NO供体，如S-亚硝基半胱氨酸（S-NC）和硝酸甘油（NTG）；过氧亚硝酸盐生成剂，如3-吗啉代 sydnonimine（SIN-1）；过氧亚硝酸盐抑制剂，如超氧化物歧化酶加过氧化氢酶（SOD/Cat）；以及NOS抑制剂，如N(G)-硝基-L-精氨酸甲酯（L-NAME）对正常和缺血性耳蜗的作用。通过测量外淋巴中的亚硝酸盐/硝酸盐来表明缺血20至120分钟后耳蜗中NO的水平。从这些实验中收集的证据表明，NO或过氧亚硝酸盐不一定对听觉毛细胞具有破坏性，事实上，外源性NO可能在缺血条件下保护耳蜗中的神经结构免受损伤。
