Ischemic damage increases nitric oxide production via inducible nitric oxide synthase in the cochlea
Ischemic damage increases nitric oxide production via inducible nitric oxide synthase in the cochlea
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DOI：
10.1016/j.neulet.2005.08.038
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发表时间：
2005-12-31
影响因子：
2.5
通讯作者：
Gyo, K
中科院分区：
文献类型：
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作者：
Morizane, I;Hakuba, N;Gyo, K
本研究旨在观察短暂性耳蜗缺血7 d后耳蜗外淋巴液中一氧化氮（NO）生成的动态变化及诱导型一氧化氮合酶（iNOS）的免疫组化染色。此外，氨基胍，这是一种选择性的iNOS抑制剂，在缺血后立即给药，此后每24小时给药一次，共7天，以研究NO的产生是否依赖于iNOS通路。显着增加的氧化NO代谢产物，亚硝酸盐（NO2-）和硝酸盐（NO3-），测量在第一天使用体内微透析和在线高效液相色谱（HPLC）系统。iNOS在缺血后第1、4天呈强阳性表达，第7天恢复正常。氨基胍的管理减少了第一天的氧化NO代谢产物和抑制iNOS的表达。这些结果表明，短暂性缺血导致显着增加NO的生产外淋巴液中，这可能是由于诱导型一氧化氮合酶途径。(C)2005爱思唯尔爱尔兰有限公司保留所有权利。
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.