Address for correspondence: Run-Sheng Ruan, Department of Otolargncology, National University of Singapore, Lower Kent Ridge Road, Singapore 119074. Fax: (65) 7753820.
entrrs{at}nus.edu.sg
Ann. N.Y. Acad. Sci. 962: 260-274 (2002).
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
NG-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.
