Fechter L D, Young J S, Carlisle L
Department of Environmental Health Sciences, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
Hear Res. 1988 Jul 1;34(1):39-47. doi: 10.1016/0378-5955(88)90049-4.
Previous studies have determined that severe systemic hypoxia disrupts cochlear function acutely, but have suggested that augmentation of cochlear perfusion may successfully protect cochlear function under all but the most profound hypoxic treatments. In the current study we report on the chronic effects of simultaneous exposures to noise and carbon monoxide on pure tone thresholds and hair cell survival in rats. Following initial threshold determination, rats received acute exposure to carbon monoxide, noise, or both agents concurrently. Thresholds were evaluated 2-4 and 6-8 weeks later. The data show that carbon monoxide alone does not affect either auditory thresholds or compromise hair cells at the light microscopic level. The noise exposure alone produced variable, but quite limited permanent threshold shifts which were related to the power spectrum of the broad band noise that was employed. Hair cell loss was restricted to the basal turn of the cochlea. Simultaneous exposure to carbon monoxide and noise induced large threshold shifts at all frequencies studied, but the effect was greatest at the highest test frequency; an effect not consistent with the noise power spectrum. Widespread hair cell loss persisted over fully half of the basilar membrane in the most severely affected rat. Outer hair cells appear to be particularly vulnerable. Carbon monoxide plus noise did not appear to preferentially disrupt a particular row of outer hair cells. These data complement existing evidence that hyperoxia can mitigate against noise induced injury and reinforce the view that some types of noise induced damage may result from metabolic insufficiencies.
以往的研究已确定，严重的全身性缺氧会急性破坏耳蜗功能，但也表明，除了极严重的缺氧处理外，增加耳蜗灌注可能成功保护耳蜗功能。在本研究中，我们报告了大鼠同时暴露于噪声和一氧化碳对纯音阈值和毛细胞存活的慢性影响。在最初确定阈值后，大鼠同时接受一氧化碳、噪声或两种因素的急性暴露。在2 - 4周和6 - 8周后评估阈值。数据显示，单独一氧化碳既不影响听觉阈值，在光学显微镜水平上也不损害毛细胞。单独的噪声暴露产生了可变但相当有限的永久性阈值变化，这与所使用的宽带噪声的功率谱有关。毛细胞损失仅限于耳蜗的基部。同时暴露于一氧化碳和噪声在所有研究频率上均引起大幅阈值变化，但在最高测试频率时影响最大；这种影响与噪声功率谱不一致。在受影响最严重的大鼠中，超过一半的基底膜上持续存在广泛的毛细胞损失。外毛细胞似乎特别脆弱。一氧化碳加噪声似乎并没有优先破坏特定排的外毛细胞。这些数据补充了现有的证据，即高氧可减轻噪声诱导的损伤，并强化了某些类型的噪声诱导损伤可能源于代谢不足的观点。
