Cochlear Dysfunction and Free Radicals : hydroxyl radicals, metallic elements, steroid hormones and SOD

金属元素：局部缺血或窒息后游离铁浓度瞬间升高。耳蜗灌注铁螯合剂可改善局部缺血后DPOAE的抑制。羟基自由基：局部缺血后，淋巴周围可识别羟基自由基的产生，并在再灌注后持续2小时或更长时间。羟基自由基清除剂可显著降低缺血后CAP的阈值偏移。类固醇激素：豚鼠耳蜗中糖皮质激素受体mRNA表达水平较高。糖皮质激素受体mRNA水平在声过度刺激后立即显著降低。耳蜗内糖皮质激素浓度高且持续时间长。一氧化氮（NO）：再灌注后检测到NO浓度明显升高。NO抑制剂可减轻局部缺血后CAP阈值偏移。

Metallic elements : Concentration of free iron transiently increased after local ischemia or asphyxia. The depression of DPOAE after local ischemia was improved by cochlear perfusion of an iron chelator.Hydroxyl radicals : The generation of hydroxyl radicals was recognized in the perilymph after local ischemia, and was continued for 2 hours or more after reperfusion. The threshold shift of CAP after ischemia was significantly reduced by administration of scavengers to hydroxyl radicals.Steroid hormones : The high level glucocorticoid receptor mRNA was revealed in the cochlea of the guinea pig. The level of glucocorticoid receptor mRNA significantly decreased immediately after exposure to the acoustic overstimulation. The concentration of glucocorticoid was high and maintained for a long period in the cochlea.Nitric oxide (NO) : Significant increase of NO concentration was recognized after reperfusion. NO inhibitors alleviated the CAP threshold shift after local ischemia.