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一过性升高。局部缺血后DPOAE的抑制通过耳蜗灌注铁螯合剂得到改善。羟基自由基：局部缺血后外淋巴中识别出羟基自由基的产生，并在再灌注后持续2小时或更长时间。羟自由基清除剂可明显降低CAP缺血后的阈值漂移。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的水平显着下降后立即暴露于声过度刺激。一氧化氮（NO）：再灌注后，耳蜗组织中NO含量显著增加。NO抑制剂可减轻局灶性脑缺血后CAP阈值漂移。

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.