Whitehead M L, Lonsbury-Martin B L, Martin G K
Department of Otolaryngology (M-805), University of Miami, Florida 33101.
J Acoust Soc Am. 1992 Nov;92(5):2662-82. doi: 10.1121/1.404382.
In a previous report, it was shown that, in normal rabbit ears, the amplitude and phase of 2f1-f2 distortion-product otoacoustic emissions (DPOAEs) elicited by low-level (< 60-70 dB SPL) stimuli display a differential dependence on stimulus parameters to those evoked by high-level (> 60-70 dB SPL) stimuli, indicating differences in the underlying generation mechanisms. In the present study, the physiological vulnerability of DPOAEs in each of the two 2f1-f2 DPOAE-response regions identified on the basis of differential parametric properties, was characterized. Thus emissions evoked using stimulus levels from 45-75 dB SPL were measured over time upon: (1) induction of lethal anoxia, (2) acute injection of ethacrynic acid, and (3) acute injection of ethacrynic acid 2 h after a single administration of gentamicin. The DPOAEs evoked by low-level stimuli (45 dB SPL) were abolished within 3-4 min of induction of anoxia, whereas DPOAEs evoked by high-level stimuli (75 dB SPL) were unchanged in this period. The high-level emissions decreased with a complex time course postmortem, and demonstrated behaviors, including evidence of susceptibility to fatigue, suggesting a dependence upon a cochlear energy supply. Low-level DPOAEs could be temporarily abolished, with complete recovery, by an acute administration of ethacrynic acid that had little effect on high-level DPOAEs. Treatment with the gentamicin and ethacrynic-acid combination, which would be expected to produce widespread hair-cell damage, eliminated low-level DPOAEs, and greatly reduced high-level emissions. In combination with previously published data, these findings strongly suggest that low- and high-level 2f1-f2 DPOAEs arise from discrete sources. The data are consistent with the proposal that the low-level DPOAE source is an active, micromechanical process, but suggest that the proposed origin of high-level DPOAEs exclusively in the passive macromechanics of the cochlear partition may be incorrect. The elimination of both low- and high-level DPOAEs revealed the presence of a third, residual 2f1-f2 DPOAE component, approximately 75-80 dB below the stimulus-tone levels, that may reflect the true passive-distortion response of the cochlea.
在之前的一份报告中显示,在正常兔耳中,低强度(<60 - 70 dB SPL)刺激诱发的2f1 - f2畸变产物耳声发射(DPOAE)的幅度和相位,与高强度(>60 - 70 dB SPL)刺激诱发的DPOAE对刺激参数的依赖性不同,这表明其潜在的产生机制存在差异。在本研究中,对基于不同参数特性确定的两个2f1 - f2 DPOAE反应区域中每个区域的DPOAE的生理易损性进行了表征。因此,使用45 - 75 dB SPL的刺激水平诱发的耳声发射随时间进行测量,测量条件如下:(1)诱导致死性缺氧;(2)急性注射依他尼酸;(3)单次给予庆大霉素2小时后急性注射依他尼酸。低强度刺激(45 dB SPL)诱发的DPOAE在缺氧诱导后3 - 4分钟内消失,而在此期间高强度刺激(75 dB SPL)诱发的DPOAE保持不变。高强度耳声发射在死后随时间呈现复杂的变化过程,并表现出包括易疲劳迹象在内的行为,这表明其依赖于耳蜗能量供应。急性给予依他尼酸可使低强度DPOAE暂时消失并完全恢复,而对高强度DPOAE影响不大。庆大霉素和依他尼酸联合治疗预期会导致广泛的毛细胞损伤,消除了低强度DPOAE,并大幅降低了高强度耳声发射。结合先前发表的数据,这些发现强烈表明低强度和高强度2f1 - f2 DPOAE来自不同的来源。数据与低强度DPOAE源是一个活跃的微机械过程的提议一致,但表明高强度DPOAE仅源于耳蜗隔的被动宏观力学这一提议可能不正确。低强度和高强度DPOAE均消失揭示了存在第三个残余的2f1 - f2 DPOAE成分,其比刺激音水平低约75 - 80 dB,这可能反映了耳蜗真正的被动畸变反应。