OTOTOXICITY OF CHEMICAL ASPHYXIANTS AND NOISE

声刺激的感受器细胞特别容易受到 由于血液的有限特性，降低了氧分压 供给内耳。电生理数据已经证明 窒息会扰乱试听，但轻微的、长期的后果 低氧对听觉系统的影响尚未被研究过。一个目标是 这项调查是为了确定亚慢性接触化学物质 与职业中普遍遇到的水平相关的窒息剂量 而环境设置会产生耳毒性。慢性和脉冲噪声 会导致听觉损伤，但这是否通过机械性损伤发生 创伤或代谢衰竭是不确定的。因为有数据 这表明噪音降低了内淋巴液中的氧分压 并对内耳产生血管损伤，已被 假设噪音导致的听力损失可能是由抑郁引起的 氧气供应情况。如果噪音确实通过限制氧气而扰乱听力 如果它损害内耳血管结构，那么它就是 合乎逻辑的假设是，噪音会增强 化学窒息暴露。这项提案的最终目标将是 说明噪音和化学窒息物质之间相互作用的性质 曝光。要使用的方法包括调制的措施 低强度测试刺激及随后的声学惊厥反射 内耳的组织学检查。

The receptor cells for acoustic stimuli are particularly vulnerable to reduced oxygen tension because of the limited characteristics of blood supply to the inner ear. Electrophysiological data have demonstrated that asphyxiation disrupts audition, but the consequences of mild, prolonged hypoxia upon the auditory system have not been investigated. One aim of this investigation is to determine whether subchronic exposure to chemical asphyxiants at doses relevant to levels widely encountered in occupational and environmental settings produces ototoxicity. Chronic and impulse noise can induce auditory damage, but whether this occurs through mechanical trauma or by metabolic exhaustion is uncertain. Because there are data which show that noise reduces oxygen tension in the endolymph fluid of the scala media and produces vascular damage to the inner ear, it has been hypothesized that noise induced auditory loss may result from depressed oxygen availability. If noise does disrupt hearing by restricting oxygen to the Corti Organ or if it damages inner ear vascular structures it is logical to assume that noise would potentiate the ototoxic effects of chemical asphyxiant exposure. The final aim of this proposal will be to specify the nature of the interaction between noise and chemical asphyxiant exposure. The methods to be used include measures of modulation of the acoustic startle reflex by low intensity test stimuli and subsequent histological examination of the inner ear.