Ischemic damage increases nitric oxide production via inducible nitric oxide synthase in the cochlea

被引：24

作者：

Morizane, I ^{[1
]}

Hakuba, N ^{[1
]}

Hyodo, J ^{[1
]}

Shimizu, Y ^{[1
]}

Fujita, K ^{[1
]}

Yoshida, T ^{[1
]}

Gyo, K ^{[1
]}

机构：

[1] Ehime Univ, Sch Med, Dept Otolaryngol, Toon, Ehime 7910295, Japan

来源：

NEUROSCIENCE LETTERS | 2005年 / 391卷 / 1-2期

关键词：

nitric oxide (NO); inducible nitric oxide synthase (iNOS); transient cochlear ischemia; aminoguanidine;

D O I：

10.1016/j.neulet.2005.08.038

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The present study was designed to elucidate the dynamic changes of nitric oxide (NO) production in the perilymph and to investigate the immunostaining for inducible nitric oxide synthase (iNOS) in the cochlea for 7 days after transient cochlear ischemia. Moreover, aminoguanidine, which is a selective iNOS inhibitor, was administrated immediately following ischemia and every 24 h thereafter for 7 days to investigate whether the production of NO is dependent on the iNOS pathway. Significant increases in the oxidative NO metabolites, nitrite (NO2-) and nitrate (NO3-), were measured on day I using an in vivo microdialysis and on-line high performance liquid chromatography (HPLC) system. The immunostaining for iNOS was strongly expressed on days I and 4 and returned to normal on day 7 after the ischemia. The administration of aminoguanidine reduced the oxidative NO metabolites on day I and suppressed the expression of iNOS. These findings suggest that transient ischemia causes a remarkable increase in NO production in the perilymph, which might be attributable to the iNOS pathway. (C) 2005 Elsevier Ireland Ltd. All rights reserved.

引用

页码：62 / 67

页数：6

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