豚鼠椎基底动脉缺血/再灌注致耳蜗损伤的iNOS表达  

Study on the changes of iNOS following vertebrobasilar artery ischemia reperfusion in guinea pigs

作　　者：刘斌[1] 任基浩[2] 葛益林[2] 

机构地区：[1]湖南省郴州市第一人民医院耳鼻咽喉-头颈外科,湖南郴州423000 [2]中南大学湘雅二医院耳鼻咽喉-头颈外科,湖南长沙410011

出　　处：《中国医学工程》2009年第4期256-258,共3页China Medical Engineering

基　　金：国家中医药管理局基金项目(No:2002LHR14)

摘　　要：目的探讨豚鼠椎基底动脉缺血/再灌注时是否存在iNOS异常表达。方法经颅底径路建立豚鼠椎基底动脉缺血/再灌注耳蜗损伤模型,采用免疫组织化学技术,对各组动物近中轴位切片行iNOS免疫组织化学染色,光学显微镜下观察在耳蜗组织中的表达情况。结果正常豚鼠耳蜗螺旋神经节、Corti's器、血管纹、螺旋韧带的细胞浆和/或细胞核内iNOS染色呈弱阳性,缺血再灌注12h可见明显表达,24h表达最强,48h表达逐渐减弱。结论iNOS在耳蜗缺血再灌注损伤出现异常表达,参与耳蜗缺血再灌注损伤。【Objective】To investigate the expression of the iNOS in the cochlea of guinea pigs induced by vertebrobasilar artery ischemia reperfusion. 【Method】The models of vertebrobasilar artery ischemia reperfusion were established via the skull base approach. The spatial and temporal features of iNOS induction following ischemia reperfusion were studied by paraflin embedded immunohistochemistry. 【Results】The positive reaction could be found in the cytoplasm of the Corti, spiral ganglion cells （SGCs）, and stria vascularis normol control group and expression of iNOS was increased in the ischemia group and ischemia reperfusion groups. The peaking time of expression was at 24 hours after ischemia. 【Conclusion】 The obvious upregulation of iNOS was observed in ischemia-reperfusion cochlea tissue, as compared to the normal control group. iNOS may be involved in the ischemia reperfusion injury.

关 键 词：耳蜗 缺血再灌注损伤 诱导型一氧化氮合酶 

分 类 号：R764.35[医药卫生—耳鼻咽喉科]