豚鼠畸变产物微音器电位与畸变产物耳声的发射的相关？…

为探讨畸变产物微间电位（ＤＰＣＭ）是否畸变产物耳声发射（ＤＰＯＡＥ）引发，将豚鼠的ＤＰＯＡＥ和ＤＰＣＭ同时叠加，发现在较高强度的声刺激下（ｆ０＝１００６Ｈｚ，ｆ０＝２０１１Ｈｚ，ｆ０＝４０３３Ｈｚ），ＤＰＣＭ叠加结果与ＤＰＯＡＥ各峰有一一对应的关系，ＣＭ的２ｆ１－ｆ２峰相对值（与ｆ１峰比值）比ＤＰＯＡＥ的２ｆ－ｆ２要小得多。较低声强刺激时（ｆ０＝１００６Ｈｚ〈５０ｄＢ，ｆ０＝２０１１Ｈｚ〈６０ｄＢ     

豚鼠外淋巴瘘对畸变产物耳声发射的影响

为观察豚鼠外淋巴瘘造模后畸变产物耳声发射（ＤＰＯＡＥ）的变化，选用１１只豚鼠右耳为实验耳，手术建立蜗窗外淋巴瘘。在实验前、打开听泡、蜗窗膜造瘘、缝合伤口及外淋巴瘘造后１８天，均以２ｆ１－ｆ２ＤＰＯＡＥ的幅值记录其变化。测试完毕后豚鼠耳蜗行火棉胶包埋切片，观察形态学改变。结果发现在形成蜗窗膜外淋巴瘘前后ＤＰＯＡＥ幅值变化差异有显著性（Ｐ＜０．０１），１８天后蜗窗膜愈合者ＤＰＯＡＥ幅值明显提高，接近实验前，而未愈合者则下降明显。病理检查见Ｃｏｒｔｉ器正常，愈合的蜗窗膜有上皮增生，肉芽及纤维母细胞。豚鼠形成外淋巴瘘后ＤＰＯＡＥ幅值明显下降，愈合后又上升，提示ＤＰＯＡＥ可作为外淋巴瘘辅助诊断的手段之一。     

自由基清除剂二甲基亚砜对庆大霉素耳蜗毒性的影响

观察豚鼠同时注射二甲基亚砜（ＤＭＳＯ）与庆大霉素（ＧＭ）及单独注射ＧＭ等几组动物后，耳蜗听功能、扫描电镜所见及耳蜗和血清中脂质过氧化物（ＬＰＯ）丙二醛（ＭＤＡ）含量的变化。结果表明ＧＭ＋ＤＭＳＯ组动物ＡＰ阈值较ＧＭ组明显降低，ＡＰ（Ｎ＿１）潜伏期ＧＭ组较ＧＭ＋ＤＭＳＯ组显著延长，耳蜗扫描电镜显示ＧＭ＋ＤＭＳＯ组毛细胞受损程度较ＧＭ组明显为轻。耳蜗中ＭＤＡ检测表明，ＧＭ组耳蜗中ＭＤＡ含量较ＧＭ＋ＤＭＳＯ组明显增高（Ｐ＜０．０１）。提示自由基引起耳蜗ＬＰＯ可能是ＧＭ耳毒性机制之一；ＤＭＳＯ可减轻ＧＭ的耳毒性。     

豚鼠外淋巴瘘对畸变产物耳声发射的影响

为观察豚鼠外淋巴瘘造模后畸变产物耳声发射的变化，选用１１只豚鼠右耳为实验耳，手术建立蜗窗外淋巴瘘。在实验前，打开听泡，蜗窗膜造瘘，缝合伤口及外淋巴瘘造后１８天，均以２ｆ１－ｆ２ｚＤＰＯＡＥ的幅值记录其变化。测试完毕后豚鼠耳蜗行火棉胶包埋切片，观察形态学改变。结果发现在形成蜗窗膜外淋巴瘘前后ＤＰＯＡＥ幅值变化差异有显著性（Ｐ〈０．０１），１８天后蜗窗膜愈合者ＤＰＯＡＥ幅值明显提高，接近实验前，而未愈     

士的宁阻断橄榄耳蜗束对豚鼠畸变产物耳声发射的影响

为探讨豚鼠听觉中枢对畸变产物耳声发射（ＤＰＯＡＥ）的影响，利用士的宁阻断听觉系统的传出神经，系统观察了阻断前后ＤＰＯＡＥ的变化。结果发现在本实验条件下，所有豚鼠均可引出ＤＰＯＡＥ，在同等刺激强度和Ｌ１＝Ｌ２的情况下，低频ｆ０＝１００６Ｈｚ的ＤＰＯＡＥ强度大，而较高频ｆ０＝２０１１和ｆ０＝４０３３的ＤＯＰＡＥ强度较小。士的宁阻断橄榄耳蜗束对ＤＰＯＡＥ无影响，提示在正常神经张力下中枢不参与、不影响ＤＯ     

正常清醒豚鼠的畸变产物耳声发射特性

目的 研究正常清醒豚鼠的畸变产物耳声发射（ＤＰＯＡＥ）的特性。方法 采用ＣＥＬＥＳＴＡ ５０３型耳声发射分析仪对２６只正常清醒豚鼠（３５耳）进行ＤＰ图及ＤＰ输入／输出曲线（ＤＰ－Ｉ／Ｏ）的测试，随机选择１１只正常清醒豚鼠（２０耳）进行ＤＰＯＡＥ的重复测试，用ＳＰＳＳ１０．０对数据进行统计分析。结果 在ＤＰ图中，当初始音强度Ｌ１／Ｌ２为 ７０／６５ ｄＢ ＳＰＬ时，正常清醒豚鼠的 ＤＰＯＡＥ幅值随测试频率ｆ０从０．７５－８ｋＨｚ的增加而逐渐升高（２７．９０±１．９６－5０．６５±０．７１）。在 ＤＰ－Ｉ／Ｏ中，当ｆ０分别为４、６、８ ｋＨｚ时，正常清醒豚鼠的ＤＰＯＡＥ幅值随Ｌ１／Ｌ２从７０／６５以５ｄＢ－挡降至１５／１０ ｄＢ ＳＰＬ而呈线性下降（Ｐ＜０．０１），在Ｌ１／Ｌ２为５５／５０或６０／５５ ｄＢ ＳＰＬ处出现饱和或低谷，同一Ｉ／Ｏ曲线上Ｌ１／Ｌ２分别从７０／６５及５５／５０ ｄＢ ＳＰＬ递减至阈值的Ｉ／Ｏ斜率（分别记为ＫＴ及ＫＬ）均接近于１，且ＫＬ大于ＫＴ（Ｐ＜０．０１）。重复测试的ＤＰＯＡＥ幅值差异小（＜ １ｄＢ ＳＰＬ）且无统计学意义（Ｐ＞０．０５）。结论 正常清醒豚鼠ＤＰＯＡＥ测试充分表现了其捡出率高、反应幅值大     

实验性膜迷路积水的位听功能测试

用２０只成年豚鼠进行前庭功能、听功能检查，内淋巴囊破坏后３０、６０、９０天复试，发现术后正弦摆动前庭眼震（ＳＰＶＮ）之频率明显下降，幅度无明显变化。术后短声与滤波短声１６ＫＨＺ－０．２５ｋＨｚ诱发的复合动作电位（ＣＡＰ）阈值均提高。畸变产物耳声发射（ＤＰＯ）ｆ１为２０５０Ｈｚ时，术后３０天２ｆ１－ｆ２之ＤＰＯ幅度降低（Ｐ＜０．０５），术后６０天进一步下降（Ｐ＜０．０１）；且ｆ１为４０００Ｈｚ之ＤＰ     

切断听神经对豚鼠DPOAE的影响

利用手术切断听的方法分离中枢与外周耳蜗的神经联系，观察分离前后ＤＯＡＥ的变化。在本实验条件下，所有豚鼠均可引出ＤＰＯＡＥ，在同等刺激强度和Ｌ１＝Ｌ２的情况下，低频ｆｏ＝１００６Ｈｚ的ＤＰＯＡＥ强度大，而较主频ｆ０＝２０１１和ｆ０－４０３３Ｈｚ的ＤＰＯＡ强度较小，切断听神经对ＤＰＯＡＥ无影响，无噪声状态下中枢不参与、不影响ＤＰＯＡＥ的产生和形成，打开豚鼠骨大泡，可引起ＤＰＯＡＥ明显下降，经分析发现主     

豚鼠噪声暴露后畸变产物耳声发射与外毛细胞的改变

为观察豚鼠噪声暴露后畸变产物耳声发射（ＤＰＯＡＥ）与内耳毛细胞的改变，将１６只健康豚鼠分为３组，正常对照组３只，噪声后即刻组３只，７ｄ组１０只。暴露于１１５ｄＢ ＳＰＬ模拟潜艇机舱噪声中４ｈ，暴露后即刻及７ｄ检测ＤＯＰＡＥ听力图及Ｉ／Ｏ函数曲线，光镜及扫描电镜观察耳蜗毛细胞的改变。暴露即刻组ＤＰＯＡＥ振幅消失（Ｐ〈０．０１），７ｄ后又恢复至暴震前的基线水平（Ｐ〉０．０５）。光镜及扫描电镜显示耳蜗２     

耳蜗内环境改变对畸变产物耳声发射的影响

耳蜗内环境改变对畸变产物耳声发射的影响姜伟张敬人江平汪磊畸变产物耳声发射（ＤＰＯＡＥ）是诱发性耳声发射的一种，其与耳蜗内环境变化的关系尚不确定。我们利用速尿对耳蜗的毒性作用，给豚鼠静脉注射速尿后观察内淋巴电位（ＥＰ）及ＤＰＯＡＥ的改变，探讨耳蜗内环境...     

谷氨酸对豚鼠畸变产物耳声发射和听性脑干反应的影响

目的 研究外源性谷氨酸对畸变产物耳声发射(distortion product otoacoustlcemission，DPOAE)、听性脑干反应(auditory brainstem response，ABR)及耳蜗形态学的影响。方法应用豚鼠全耳蜗灌流技术，耳蜗灌流10mmol/L谷氨酸2h，分别记录灌流前、后DPOAE和ABR；耳蜗微音电位(cochlear microphonics，CM)和听神经复合动作电位(compound action potential，CAP)；应用透射电镜进行耳蜗形态学观察。结果灌流人工外淋巴液前、后CM及CAP无改变；灌流10mmol／L谷氨酸后DPOAE无改变，ABR潜伏期延长；同样灌流10mmol／L谷氨酸后CM幅度虽有下降、但是其非线性特点无改变；CAP阈值平均升高了35dB；灌流谷氨酸后内毛细胞及其下方神经纤维出现空泡。结论谷氨酸作为耳蜗主要的兴奋性传入神经递质，过度释放可以产生兴奋性毒性，损伤耳蜗内毛细胞及传入神经。同时本实验为建立听神经病的动物模型提供了一个参考方法。     

effects of glutamate on distortion-product otoacoustic emissions and auditory brainstem responses in guinea pigs

Objective To investigate changes in evoked potentials and structure of the guinea pig cochleae during whole cochlear perfusion with glutamate. Methods CM, CAP, DPOAE, and ABR were recorded as indicators of cochlear functions during whole cochlear perfusion. The morphology of the cochlea was studied via transmission electron microscopy. Results There were no significant changes in DPOAE amplitude before and after glutamate perfusion. CM I/O function remained nonlinear during perfusion. ABR latencies were delayed following glutamate perfusion. The average CAP threshold was elevated 35 dB SPL following glutamate perfusion.. The OHCs appeared normal, but the IHCs and afferent dendrites showed cytoplasmic blebs after glutamate perfusion. Conclusions While being a primary amino acid neurotransmitter at the synapses between hair cells and spiral ganglion neurons, excessive glutamate is neurotoxic and can destroy IHCs and spiral ganglion neurons. The technique used in this study can also be used to build an animal model of auditory neuropathy.     

一氧化氮在豚鼠耳蜗作用的实验研究

为探讨ＮＯ在内耳的作用，采用外淋巴给药途径，观察一氧化氮气体（ＮＯ）、Ｌ－精氨酸、硝普钠及一氧化氮合酶（ＮＯＳ）拮抗剂Ｎ－甲基－Ｌ－精氨酸对耳蜗蜗内电位（ＥＰ）、复合动作电位（ＣＡＰ）及耳蜗微音器电位（ＣＭ）的影响。结果表明，Ｎ－甲基－Ｌ－精氨酸可以使ＥＰ减小５０％，ＣＡＰ振幅降低３３％及ＣＭ振幅略有降低，在此基础上，用Ｌ－精氨酸外淋巴灌流可以逆转Ｎ－甲基－Ｌ－精氨酸所致的改变。ＮＯ持外淋巴缓释能     

一氧化氮在豚鼠耳蜗作用的实验研究

为探讨ＮＯ在内耳的作用，采用外淋巴给药途径，观察一氧化氮气体（ＮＯ）、Ｌ－精氨酸、硝普钠及一氧化氮合酶（ＮＯＳ）拮抗剂Ｎ－甲基－Ｌ－精氨酸对耳蜗蜗内电位（ＥＰ）、复合动作电位（ＣＡＰ）及耳蜗微音器电位（ＣＭ）的影响。结果表明，Ｎ－甲基－Ｌ－精氨酸可以使ＥＰ减小５０％，ＣＡＰ振幅降低３３％及ＣＭ振幅略有降低，在此基础上，用Ｌ－精氨酸外淋巴灌流可以逆转Ｎ－甲基－Ｌ－精氨酸所致的改变。ＮＯ持续外淋巴缓释能使Ｎ－甲基－Ｌ－精氨酸导致的ＥＰ、ＣＡＰ及ＣＭ的改变恢复，并超过正常，随之出现快速下降。外淋巴灌流硝普钠后，ＥＰ、ＣＡＰ及ＣＭ短暂升高后逐渐下降，并维持在较低水平。ＣＡＰＮ１波及ＣＭ潜伏期的变化规律与其振幅的变化规律基本一致。结果提示，ＮＯ在生理条件下维持内耳功能，可能参与耳蜗毛细胞微机械特性及敏感性的调节，过量表达可以产生耳蜗毒性     

豚鼠畸变产物耳声发射潜伏期的对侧抑制效应现象

目的 通过观察对侧抑制效应中畸变产物耳发射（distortion productotoacousticemissions,DPOAE)各指标的改变,探讨耳蜗生理机制及传出神经的调节机能。方法 12只健康杂色豚鼠分A、B2组,在对侧耳无声刺激及给予70dB SPL宽带噪声条件下,分别使用不同的原始纯音强度组合测定在f2＝2、4、6kHz时测试耳DPOAE之幅值及潜伏期。次日,A组动物背侧径路开放右耳听泡,圆窗膜给予60mmol/L卡因酸1μL,作用3h后拭去。给药后6h测试右耳无声刺激和给予70dB SPL宽带噪声刺激下,左耳的DPOAE幅值、潜伏期等指标。结果 ①用药前,A组对侧耳给声时以等强度原始音诱发的测试耳DPOAE各频率幅值与给声前基本无变化,而潜伏期显著延长;②用药前,B组对侧耳给声以差强度原始音（L2＝L1－10dB)诱发的测试耳DPOAE在2、4kHz的幅值与给声前相比有显著减小,潜伏期也显著延长;③A组用药后,对侧耳给声对测试耳DPOAE幅值和潜伏期均无显著影响。结论 潜伏期亦是对侧抑制研究中的敏感指标。对侧抑制效应在调制耳蜗转导机制中发挥负反馈作用。     

Effect of inner and outer hair cell lesions on electrically evoked otoacoustic emissions

When the cochlea is stimulated by a sinusoidal current, the inner ear emits an acoustic signal at the stimulus frequency, termed the electrically evoked otoacoustic emission (EEOAE). Recent studies have found EEOAEs in birds lacking outer hair cells (OHCs), raising the possibility that other types of hair cells, including inner hair cells (IHCs), may generate EEOAEs. To determine the relative contribution of IHCs and OHCs to the generation of the EEOAE, we measured the amplitude of EEOAEs, distortion product otoacoustic emissions (DPOAEs), the cochlear microphonic (CM) and the compound action potential (CAP) in normal chinchillas and chinchillas with IHC lesions or IHC plus OHC lesions induced by carboplatin. Selective IHC loss had little or no effect on CM amplitude and caused a slight reduction in mean DPOAE amplitude. However, IHC loss resulted in a massive reduction in CAP amplitude. Importantly, selective IHC lesions did not reduce EEOAE amplitude, but instead, EEOAE amplitude increased at high frequencies. When both IHCs and OHCs were destroyed, the amplitude of the CM, DPOAE and EEOAE all decreased. The increase in EEOAE amplitude seen with IHC loss may be due to (1) loss of tonic efferent activity to the OHCs, (2) change in the mechanical properties of the cochlea or (3) elimination of EEOAEs produced by IHCs in phase opposition to those from OHCs.     

顺铂中毒后豚鼠耳蜗电位变化的特征及形态学实验观察

目的 观察顺铂对耳蜗微音电位（ＣＭ）、总和电位（ＳＰ）及复合动作电位（ＣＡＰ）的影响及毛细胞形态学改变。方法 用人工外淋巴液和顺铂灌流豚鼠耳蜗，分别记录耳蜗第三回中阶的ＣＭ、－ＳＰ及ＣＡＰ，琥珀酸脱氢酶染色观察毛细胞的数量变化，透射电镜观察外毛细胞结构。结果 顺铂灌流１ｈ：≤６０ｄＢ ＳＰＬ声强级刺激时ＣＭ、－ＳＰ和ＣＡＰ幅度均较灌流顺铂前略下降，≥７０ｄＢ ＳＰＬ声强级刺激时幅度比灌流顺铂前明显     

钙泵间接激活剂对噪声性聋的保护作用

OBJECTIVE: To investigate the possible protective effect of phorbol-12-myristate-13-acetate (PMA), an activator of protein kinase C (PKC) and indirect activator of Ca2+ pump, on noise-induced hearing loss (NIHL). METHODS: Twenty guinea pigs were divided randomly into two groups, and then perfused with artificial perilymph solutions in one group and with artificial perilymph solutions containing 3 mumol/L PMA in the other one, respectively. All animals were exposed with 100 dB SPL white noise for 2 hours. Cochlear microphonics (CM) and compound action potential (CAP) were recorded from the round window (RW) before noise exposure and 2 hours after noise exposure. RESULTS: There was no significant difference in CAP threshold and CM amplitude between two groups before noise exposure. A significant difference was observed in CAP threshold and CM amplitude between two groups after noise exposure. The amplitude of CM decreased and the threshold of CAP increased in both group after noise exposure, but in the PMA group the decrease of the amplitude of CM was higher while the increase of threshold of CAP lower than that in control (P < 0.05). CONCLUSION: PMA might have partly protective effect on NIHL. These findings indirectly proved that intracellular Ca2+ overload might involve in the mechanism of NIHL.     

Nitrosoglutathione suppresses cochlear potentials and DPOAEs but not outer hair cell currents or voltage-dependent capacitance

Biochemical and pharmacological evidence support a role for nitric oxide (NO) and glutathione (GSH) in the cochlea. GSH combines with NO in tissue to form nitrosoglutathione (GSNO) that can act as a storage form for GSH and NO. Therefore, we tested GSNO on sound-evoked responses of the cochlea (cochlear microphonic, CM; summating potential, SP; compound action potential, CAP; cubic distortion product otoacoustic emission, DPOAE), on the endocochlear potential (EP), on isolated outer hair cell (OHC) currents and voltage-dependent capacitance, and on Deiters' cell currents. In vivo application of GSNO in increasing concentrations reversibly reduced low-intensity sound-evoked CAP, SP and DPOAEs starting at about 1 mM (CAP) and 3.3 mM (SP, DPOAE). However, even at 10 mM, GSNO had little effect on the EP. In vitro, salicylate (10 mM) but not GSNO (3 and 10 mM) suppressed the early capacitative transients of OHCs. GSNO (3 and 10 mM) had no effect on the whole cell currents of OHCs or Deiters' cells. Results show that GSNO suppresses cochlear function. This suppression may be due to an effect of GSNO on the cochlear amplifier. The actions of GSNO were different from those of other NO donors; therefore, the effects of GSNO may not be mediated by NO. The mechanisms underlying GSNO effects seem to be different from those of salicylate.     

Fine alterations of distortion-product otoacoustic emissions after moderate acoustic overexposure in guinea pigs

Guinea pigs were exposed to a pure tone at 6 kHz and 80 dB SPL for 30 minutes in order to induce mild reversible auditory fatigue over the 4 hours following exposure. Cochlear monitoring aimed to compare the shifts in round-window compound action potentials (CAP) thresholds to those of 2f1-f2 distortion-product otoacoustic emissions (DPOAE, frequency of stimuli f1 and f2). Both responses were evaluated every 1/10th octave between 6 and 12 kHz for CAP thresholds, and from 4 to about 14 kHz for DPOAEs in response to 50- and 70-dB SPL stimuli. The auditory fatigue turned out to be sufficiently mild that DPOAEs remained present, so that their microstructure could be followed up while the stimulus frequency ratio f2/f1 was swept from 1.06 to 1.30 (fixed f2) so as to derive DPOAE level profiles against f2/f1 and group latencies. CAP thresholds decreased by about 10 dB above 7.2 kHz, whereas DPOAE amplitudes decreased at most f2 frequencies from 6.6 kHz to 15.2 kHz, with the range of decrease being slightly narrower at higher stimulus intensities. While the mean DPOAE shift after 1 hour was around 5 dB irrespective of stimulus intensity, it tended to increase slightly after 2 hours despite stable CAP thresholds. DPOAE profiles against f2/f1 were slightly modified by the auditory fatigue, so that the maximum tended to be reached at lower ratio. No significant variation of DPOAE latencies was found after acoustic overstimulation. These experiments show that complex DPOAE changes were induced by auditory fatigue and their relationship to CAP threshold changes does not seem to be straight-forward. Nonetheless, fine DPOAE recordings might be useful to detect early changes in cochlear mechanics.