脉冲噪声暴露后大鼠听皮层神经颗粒素的表达研究

目的揭示脉冲噪声暴露后不同时期大鼠听皮层神经颗粒素(neurogranin,Ng)表达的变化。方法将50只成年SD大鼠随机分为5组:正常对照组及脉冲噪声暴露后3、7、14、28天组,每组10只。脉冲噪声暴露条件为:平均压力峰值156dB SPL,脉宽为0.25ms,暴露50次,每次间隔6s。于噪声暴露前及噪声暴露后即刻、3、7、14、28天检测各组大鼠ABR反应阈,同时,应用Western blot方法检测各组大鼠听皮层中的Ng的含量。结果与对照组相比,各组大鼠噪声暴露后即刻、3、7、14、28天各频率ABR反应阈均明显提高(P<0.05),噪声暴露后第7天,各频率ABR阈值有所恢复,第14天时趋于稳定;与对照组(0.68±0.08)比较,噪声暴露后第3、7、14天组大鼠听皮层中Ng的含量分别为0.96±0.05、1.11±0.05、0.78±0.04,显著高于对照组,第28天组为0.36±0.03,显著低于对照组,差异均有统计学意义(P<0.05)。结论噪声暴露后,大鼠ABR反应阈明显升高,听皮层Ng的表达呈现一个先上升后降低的过程,提示脉冲噪声刺激对大鼠听觉系统产生了一定持续性的影响,听皮层出现突触可塑性变化。     

西地那非对豚鼠噪声性听觉损伤阈移的影响

目的 探讨西地那非(sildenafil)对豚鼠噪声性听觉损伤阈移的影响.方法 将豚鼠按随机数字表法分为对照组、噪声暴露组和西地那非给药组,每组10只.西地那非组及噪声组豚鼠在白噪声(A计权声压级110 dB)暴露1周后分别腹腔注射西地那非10 mg/(kg·d)及生理盐水4mL/(kg·d),连续给药4周.分别测试噪声暴露前1日、噪声暴露后1、2及4周听性脑干反应(ABR)阈值,并通过扫描电镜观察噪声暴露后4周豚鼠耳蜗毛细胞的形态变化.结果 噪声暴露1后,噪声暴露组豚鼠ABR阈值(声压级)平均提高19.1 dB,随着时间推移,阈移逐渐加大,暴露后4周,阈值平均提高22.0 dB;西地那非组噪声暴露后ABR阈值提高19.8 dB,给药后阈移逐渐减小,给药后4周,阈值仅平均提高4.8 dB.西地那非组与噪声暴露组相比,除噪声暴露结束后这一时间点以外,其余给药后各时间点ABR阈值差异均具有统计学意义(P值均＜0.05).扫描电镜显示,噪声组豚鼠耳蜗内、外毛细胞均出现听毛紊乱、融合及缺失;而西地那非组耳蜗病变较轻,听毛仅有轻微倒伏、融合现象.结论 西地那非能够减轻噪声对豚鼠耳蜗毛细胞的损害,降低噪声性听觉损伤引起的ABR阈值升高.     

脉冲噪声暴露后大鼠下丘核生长相关蛋白-43表达的研究

目的 探讨脉冲噪声暴露对大鼠下丘核生长相关蛋白-43(growth associated protein,Gap-43)表达的影响.方法 SPF级成年雄性SD大鼠30只,随机分为正常对照组6只、噪声暴露组24只,正常对照组不接受噪声暴露,噪声暴露组接受脉冲噪声暴露,噪声平均压力峰值156 dB SPL,脉宽0.25 ms,单次暴露6 s,共暴露50次.于噪声暴露前及暴露后3、7、14、28 d分别测试对照组及噪声暴露组(每个时间点6只)大鼠听性脑干反应(auditory brainstem response,ABR)阈值;然后取双侧下丘进行免疫组化染色,通过灰度值检测各组大鼠下丘Gap-43蛋白表达水平.结果 噪声暴露后各组大鼠ABR反应阈显著高于正常组(P<0.01),噪声暴露后14、28 d组ABR阈值显著低于暴露后3 d组(P<0.05);噪声暴露后各组大鼠双侧下丘Gap-43蛋白表达显著高于正常组(P<0.01),暴露后28 d组大鼠下丘Gap-43蛋白表达显著低于暴露后3 d组(P<0.05).结论 脉冲噪声暴露可导致大鼠ABR反应阈显著升高,下丘Gap-43蛋白高表达;脉冲噪声暴露后不同时间大鼠ABR阈值升高和下丘Gap-43蛋白高表达的变化规律可能与听皮层突触重塑有关.     

脉冲噪声暴露后大鼠频率特异性听性脑干反应变化特点及意义

目的探讨脉冲噪声暴露后不同时间大鼠频率特异性听性脑干反应变化特点及意义。方法成年SD大鼠50只分为5组:正常组及脉冲噪声暴露后3、7、14、28天组,每组10只。脉冲噪声条件为:平均压力峰值为156dBSPL,脉宽0.25ms,暴露50次,分别于暴露前后对大鼠行ABR检测,刺激声为短音(tonepip),频率范围为2～32kHz。结果①正常大鼠2、4、8、16、32kHz的平均听阈分别为68.5±2.67、58.2±2.58、39.3±3.33、37.5±2.95、37.3±3.60dBSPL;②与脉冲噪声暴露前相比较,暴露后各组2、4、8、16、32kHzABR阈值均明显提高,差异有统计学意义(P<0.05),其中高频阈移的幅度较低频阈移幅度大;在暴露后恢复第7天时,各频率ABR阈值有所恢复,第14天时恢复明显,第28天时与第14天接近。结论脉冲噪声暴露后大鼠频率特异性听性脑干反应阈值升高,第7天后开始有所恢复,可为后期进一步研究听觉中枢可塑性建立稳定有效的急性声损伤动物模型。     

小型猪听性脑干反应分析及脉冲噪声暴露后的变化

目的了解健康小型猪的听性脑干反应特征,以及脉冲噪声暴露后其听性脑干反应的变化特点。方法健康小型猪分别给予30、50、80及100次脉冲噪声暴露,并于噪声暴露前以及暴露后即刻、1、2、4、8周进行听性脑干反应测定,了解其听性脑干反应特征及变化情况。结果健康小型猪的听性脑干反应波形包括五个典型的波峰,与其他物种一致。短声刺激下其阈值平均为25±5 d B SPL。高强度脉冲噪声暴露后,其听性脑干反应阈值显著提高。50次以上暴露即可导致无法引出可识别的听性脑干反应波形。其纯音听性脑干反应阈值在4、8、16、20k Hz和32k Hz频率也于暴露后增高。暴露后即刻,各实验组阈值均大于90 d B SPL。暴露后1周,各实验组动物ABR阈值都有不同程度的恢复,但暴露后1周内恢复较快,第2至第8周时,听阈位移趋势基本稳定。噪声暴露后1至8周,ABR阈值在4k Hz,8k Hz,16k Hz、20k Hz和32k Hz频率恢复趋势与短声刺激一致,各频率ABR阈值比较差异无统计意义。随着时间的延长,在不同频率区间内,虽然存在听阈的阈移,但是ABR波形分化较差。讨论小型猪ABR波形与啮齿类及人类相似,但小型猪ABR对脉冲噪声的敏感性较啮齿类动物更强,且恢复期更短。此外,由于小型猪与人类在基因、解剖及病理生理学上都具有较高的相似性,因此可能是听觉研究方面理想的大型哺乳动物模型。     

慢性噪声暴露对大鼠听皮层及海马脑区胰岛素样生长因子－1表达的影响

目的：观察慢性噪声暴露后大鼠听皮层及海马脑区胰岛素样生长因子－1（insulin－like growth fac-tor－1,IGF－1）的表达,探讨其在长期噪声性中枢神经系统损伤中的作用。方法成年健康雄性 Wistar 大鼠16只,随机分为噪声组和对照组各8只,噪声组暴露于100 dB SPL 白噪声28天,每天4小时,制成慢性噪声暴露模型,对照组不予任何处理。造模结束后检测两组大鼠 ABR 反应阈,并采用免疫组织化学染色方法检测 IGF－1在听皮层和海马的表达。结果噪声组造模结束后 ABR 反应阈（80．62±4．58 dB SPL）较对照组（38．75±3．54 dB SPL）明显升高（P＜0．05）,听皮层及海马脑区 IGF－1阳性神经元数目和表达强度均较对照组显著增加（P＜0．05）。结论慢性噪声暴露可以使听皮层及边缘系统海马脑区 IGF－1表达增高,这可能与其对中枢神经系统噪声性损伤的保护作用有关。     

用于毛细胞再生研究的噪声性聋动物模型的建立

目的观察高强度脉冲噪声暴露后豚鼠听功能及耳蜗结构的变化,探讨用于毛细胞再生研究的噪声性聋动物模型的建立方法。方法健康成年白色红目豚鼠50只,雌雄不限,体重250～300g。随机分成2组,正常对照组10只,噪声暴露组40只。给予脉冲噪声（压力峰值为175．0dB SPL,脉宽0．25ms,间隔时间20秒）连续暴露200次。于噪声暴露前及暴露后1周、4周、8周检测听性脑干反应（auditory brainstem respons,ABR）,毛细胞计数及耳蜗铺片免疫组化观察耳蜗结构变化。结果高强度脉冲噪声暴露后1周,40只豚鼠中有21只（52．5％）双耳各频率ABR阈值≥95dBSPL。继续观察至噪声暴露后4周及8剧,ABR阈值没有恢复,1周、4周、8周各频率ABR阈值比较无统计学差异（P〉0．05）。毛细胞计数结果显示,噪声暴露敛极重度聋后1周,内毛细胞平均缺失率为91．4％,外毛细胞平均缺失率为97．2％。免疫组化染色分析结果显示,噪声暴露致聋后1周,内、外毛细胞胞核大部分缺失,内毛细胞内侧及外毛细胞外侧的支持细胞的胞核存存。结论高强度脉冲噪声暴露可造成豚鼠极重度感音神经性聋,耳蜗毛细胞广泛缺失且无法内行恢复,而支持细胞夫部分仔留,是进行毛细胞再生研究的理想动物模型。     

依达拉奉对豚鼠耳蜗急性声损伤的保护作用

目的 探讨自由基清除剂依达拉奉对豚鼠耳蜗急性声损伤的保护作用.方法 48只白色红目雌性豚鼠随机分为6组.A组(空白对照组):不做任何处置,单纯检测听功能和耳蜗自由基含量;B组:鼓室注射生理盐水;C组:鼓室注射依达拉奉;D组:单纯噪声暴露;E组:噪声暴露+静脉注射依达拉奉;F:噪声暴露+鼓室注射依达拉奉.D、E、F组在声压级125 dB的稳态噪声暴露前2 d及暴露2 h后即刻、2、6、12、24、48和72 h检测听功能和耳蜗自由基含量.听功能检测为听性脑干反应(ABR),自由基检测采用电子顺磁共振(electron spin resonance,ESR)技术.比较各组动物在不同时间点ABR阈移及自由基含量的变化.结果 急性声损伤后豚鼠ABR阈值明显升高,与空白对照组比较,差异具有统计学意义(P<0.05),暴露后72 h仍未恢复正常.鼓室注射依达拉奉可使阈值下降约10 dB,而静脉注射则无此作用.空白对照组豚鼠耳蜗自由基值为21.68(cm/g),急性声损伤后耳蜗自由基含量明显增加,在噪声暴露后2 h达峰值,至观察结束时仍未恢复正常.静脉注射依达拉奉组对噪声损伤后耳蜗自由基生成未见明显抑制作用,而鼓室注射组则可明显抑制自由基产生.结论 经鼓室局部应用依达拉奉,对豚鼠急性声损伤后的耳蜗听觉功能具有保护作用,其机制可能与有效清除局部自由基有关.     

模拟中长期微重力和噪声环境对大鼠听功能及内耳毛细胞凋亡的影响

目的 研究模拟中长期微重力和噪声环境对大鼠听功能及内耳细胞凋亡的影响.方法 36只SD大鼠随机分为两组:空白组(6只)和实验组(30只).实验组给予持续尾部悬吊模拟微重力及飞船舱内噪声(稳态噪声+脉冲噪声)暴露,分别于悬吊及暴露前、悬吊及暴露3天、1周、2周、4周和8周后检测双耳ABR反应阈,并于悬吊及暴露3天、1周、2周、4周和8周取实验动物耳蜗行免疫组化染色观察半胱氨酸天冬氨酸蛋白酶3(caspase-3)在内耳的表达.空白组不做任何处理,常规饲养,于实验前及实验3天、1周、2周、4周和8周分别检测双耳ABR反应阈,并于饲养8周后取耳蜗行免疫组化染色观察.结果 实验前两组大鼠ABR反应阈差异无统计学意义(P＞0.05).实验组大鼠悬吊及噪声暴露后各时间点ABR反应阈较空白组均明显增高(P＜0.01),悬吊及暴露4周实验组大鼠ABR反应阈为90.00±4.26 dB SPL,明显高于3天、1周、2周及8周时(P＜0.05);悬吊及暴露8周大鼠ABR反应阈(80.00±5.22 dB SPL)有所下降,与暴露2周(85.00±4.77 dB SPL)、4周大鼠比较差异有统计学意义(P＜0.01).悬吊及噪声暴露后大鼠内耳细胞caspase-3的表达较空白组明显增强,且在一定时间内随暴露时间的延长其表达有逐渐增强的趋势,尤以悬吊及暴露4周时最明显,暴露8周时其表达强度较4周时明显下降.结论 模拟中长期微重力和噪声环境对大鼠的听功能有明显损伤,且与内耳细胞凋亡呈相同的趋势;微重力和噪声因素造成的听功能损伤可能与内耳细胞的凋亡有关.     

雌激素对豚鼠风洞噪声性听功能损伤及内耳Caspase-3表达的影响

目的探讨风洞噪声环境对豚鼠听功能及内耳毛细胞、螺旋神经节细胞上凋亡标志物Caspase-3表达的影响,并通过噪声暴露前给予预防用腹腔注射雌激素研究雌激素对噪声暴露后豚鼠听力损伤及内耳凋亡的保护作用。方法 42只豚鼠随机分为3组,其中对照组6只,单纯噪声组(噪声组)及噪声+雌激素预防组(雌激素组)各18只。两实验组暴露于模拟风洞噪声环境中。分别于噪声暴露前(Pr)、暴露后1天(E1)、3天(E3)、7天(E7)、恢复后3天(R3)、7天(R7)检测其双侧听性脑干反应阈值(ABR)。并于E3、E7、R7时间点取实验动物耳蜗行连续冰冻切片,利用免疫组织化学染色方法显示凋亡标志物Caspase-3在实验动物内耳毛细胞及螺旋神经节细胞上的表达。结果 E1、E3、E7时间点,噪声组ABR阈值较噪声暴露前明显增高(P<0.01),且暴露时间越长,ABR阈值增高越明显。雌激素组在E1的ABR阈值较噪声暴露前明显增高(P<0.01),E3和E7时ABR阈值有增高趋势,但统计学分析无显著性差异(P>0.05)。两实验组间噪声暴露后听阈变化值在E1和E3点没有统计学差异(P>0.05),在E7点统计学有显著差异(P<0.01)。R3点较E7点,噪声组ABR阈值降低(P<0.05)。雌激素组在R3时间点,ABR阈值明显降低(P<0.01),与R7点比较未见显著性差异(P>0.05);两实验组间比较雌激素组的实验动物ABR阈值降低情况明显优于噪声组(P<0.01)。噪声暴露后,豚鼠内耳螺旋神经节细胞及毛细胞的凋亡标志物Caspase-3表达在各时间段均高于对照组,且随着暴露时间的延长逐渐增高。雌激素组Caspase-3表达变化有相同趋势,但在E3、E7及R7三时间点均弱于噪声组。结论豚鼠暴露于风洞噪声环境下可导致其听功能损伤,损伤程度在本研究噪声暴露时间内与噪声累积量呈正相关。噪声暴露结束后,听力损失可部分恢复。同时,内耳凋亡标志物的表达和听力下降呈现相同趋势。噪声暴露前预防性应用雌激素,可促进噪声暴露后听力损伤的恢复、减少内耳凋亡标志物表达、减轻内耳细胞凋亡。     

模拟飞船舱内中长期失重及噪声复合因素对大鼠听器官的影响

目的　探讨模拟飞船舱内2～8周的中长期失重及噪声复合因素对大鼠脑干诱发电位和耳蜗结构的影响。方法　健康成年大鼠随机分成雄性实验及对照组、雌性实验及对照组。实验组暴露于模拟失重及稳态噪声环境中,实验结束前给予脉冲噪声暴露;对照组不施加因素。分别于实验前、实验第2、4、8周及脉冲噪声暴露后检测双侧听性脑干反应阈值（ABR）,并行扫描电镜观察。结果　两实验组内脉冲噪声暴露后ABR阈值明显增高（P 均＜0.05）;实验后2、4周ABR阈值雌性实验组均较雄性实验组低（P 均＜0.05）,扫描电镜观察发现内外毛细胞缺失,大片倒伏,随着复合因素作用时间延长耳蜗毛细胞病理性改变加重。结论　中长期失重噪声复合因素可造成大鼠听功能损害,且脉冲噪声比稳态噪声更明显;损害存在性别差异;大鼠耳蜗毛细胞病理性改变随复合因素时间延长而加重。     

Effects of alcohol and noise on temporary threshold shift in Guinea pigs

The purpose of this study was to investigate the effects of concomitant exposure to noise and alcohol on the auditory thresholds. Twenty-four guinea pigs were equally divided into three groups: the acute intoxication group, the chronic intoxication group and the control group. Animals in the acute group received single intraperitoneal injections of ethanol (2 g/kg). In the chronic group, alcohol was administered via drinking water (10%, v/v) over a 60-day period. All animals were exposed to a white noise at the intensity of 105 dB A for 30 min. Auditory brainstem response (ABR) thresholds and distortion product otoacoustic emission (DPOAE) levels were measured before, immediately after noise exposure and also 1, 2, and 7 days following exposure. The results showed: first, acute alcohol injection caused a significant, temporary elevation of ABR threshold (4.8 dB in average), while chronic alcohol treatment did not change auditory threshold significantly. Second, noise exposure induced a mean threshold shift of 15.4- 19.7 dB. ABR threshold returned to normal 2 days after exposure. Both acute and chronic alcohol treatment did not alter the magnitude and time course of recovery of the temporary threshold shift (TTS). Third, the mean DPOAE amplitudes decreased at most frequencies following acute injection of alcohol. However, the differences did not reach statistical significance. Fourth, the mean DPOAE levels dropped 3.4-9.6 dB in all groups after noise exposure and returned to normal 1 day to 2 days after noise. There were no significant differences in the amount of DPOAE suppression after noise between the three groups. In summary, we have found that acute and chronic treatment of alcohol in combination with noise did not significantly exacerbate TTS or decrease DPOAE amplitudes relative to noise exposure alone.     

模拟失重及飞船内稳态噪声对大鼠听功能的影响

目的 探讨模拟失重及飞船舱内中等强度稳态噪声对大鼠听功能影响的时效关系.方法 96只雄性SD大鼠随机分为失重组、噪声组、失重+噪声组和对照组,各24只鼠,每组大鼠再按暴露时间随机分为1周、4周组,各12只鼠,最后在暴露结束后即刻(P0)测听并处死一半大鼠作为暴露即刻组,另一半脱离暴露环境7d后(P7)测听并处死作为恢复...     

睫状神经营养因子防治强脉冲噪声对豚鼠内耳损伤的实验研究

目的探索应用睫状神经营养因子（ｃｉｌｉａｒｙｎｅｕｒｏｔｒｏｐｈｉｃｆａｃｔｏｒ,ＣＮＴＦ）防治强脉冲噪声对豚鼠内耳损伤的可能性,为强脉冲噪声致聋的防治提供新的方法。方法制作强脉冲噪声致聋豚鼠模型３６只,１８只应用ＣＮＴＦ肌内注射３周,１８只等量的生理盐水作对照,正常对照豚鼠１８只,进行耳蜗铺片计算机图像分析毛细胞计数,螺旋神经节细胞计数、耳蜗乙酰胆碱酯酶染色铺片观察和ＡＢＲ反应阈测定。结果正常对照组、噪声暴露后２１ｄ的生理盐水对照组和ＣＮＴＦ组耳蜗毛细胞平均总数（ｘ±ｓ,下同）分别为９０９４±１０３．６、７３５１±１９６．５、８５２２±２０３．１;而螺旋神经节细胞计数在耳蜗中轴切片第二回下段３组间差异有显著性,分别为５１±４．７２、２７±６．９４、３７±１０．４。乙酰胆碱酯酶染色铺片结果示ＣＮＴＦ组较生理盐水对照组耳蜗乙酰胆碱酯酶活性损失轻、范围小。结论ＣＮＴＦ在一定程度上能防止受损的螺旋神经节细胞及外毛细胞发生变性坏死,并可能促进其损伤的修复。     

The protective effects of ciliary neurotrophic factor on inner ear damage induced by intensive impulse noise]

OBJECTIVE: To evaluate the feasibility of using ciliary neurotrophic factor(CNTF) to treat intensive impulse noise-induced inner ear damage. METHODS: The guinea pigs were given either CNTF (CNTF group) or 0.9% sodium chloride (NS group) for 3 weeks after impulse noise exposure. The animals receiving neither medicine nor noise served as a control group. ABR threshold shifts, the cochlear AchE staining as well as the hair cell and spiral ganglion cell counting were carried out in three groups of animals. RESULTS: The numbers of damaged hair cells and spiral ganglion cells in the CNTF group was less than that in the NS group. AchE activity alteration was also less severe in the CNTF group. Similar to the morphological results, changes in the auditory function, represented by the ABR threshold shifts, was less in the CNTF group. CONCLUSION: CNTF can protect cochlear hair cells and spiral ganglion cells against intensive impulse noise exposure by decreasing degeneration and necrosis of the hair cells in some extent and expedite hearing recovery.     

The effect of various durations of noise exposure on auditory brainstem response, distortion product otoacoustic emissions and transient evoked otoacoustic emissions in rats

This study was designed to investigate the effect of various durations of noise exposure in animals on physiological responses from the cochlea which are also used clinically in humans: auditory brainstem response (ABR), transient evoked otoacoustic emissions (TEOAEs) and distortion product otoacoustic emissions (DPOAEs). Rats were exposed to 113 dB SPL broad-band noise (12 h on/12 h off) for durations of 3, 6, 9, 12, 15 and 21 days, and tested 24 h after cessation of the noise and again after a period of 6 weeks. ABR threshold to click stimuli and to a 2-kHz tone burst (TB), TEOAE energy content and DPOAE amplitude in the exposed rats were compared to those in a group of control rats not exposed to noise. ABR thresholds (click and TB) were significantly elevated in all exposure duration groups compared to control rats. DPOAE amplitudes and TEOAE energy content were significantly reduced. The mean ABR thresholds following 21 days exposure were significantly greater (click = 100 dB pe SPL; TB = 115 dB pe SPL) than those following 3 days exposure (click = 86 dB pe SPL; TB = 91 dB pe SPL). Linear regression analysis between recorded responses and duration of noise exposure (days) showed a significant increase in ABR thresholds of approximately 0.8-- 1.4 dB/day. TEOAE and DPOAE responses showed no such dependence on noise duration and were already maximally reduced after only 3 days of exposure. This can be explained by the possibility that short noise exposures may cause damage to the early, more active stages of cochlear transduction (as shown by TEOAEs and DPOAEs). As the noise exposure continues, further damage may be induced at additional, later stages of the cochlear transduction cascade (as shown by ABR). Thus, ABR seems more sensitive to noise duration than OAE measures.     

Chronologic changes of nitric oxide concentration in the cochlear lateral wall and its role in noise-induced permanent threshold shift

OBJECTIVE: The objective of this study was to investigate the chronologic changes of nitric oxide (NO) concentration in the cochlear lateral wall and to explore its possible role in permanent threshold shift (PTS) after intense noise exposure. MATERIALS AND METHODS: Seventeen guinea pigs were subjected to a single continuous exposure to broadband white noise at 105 +/- 2 dB sound pressure level (SPL) for 40 hours and were divided into four groups according to various postnoise recovery periods. Another 12 guinea pigs were not exposed to noise and served as controls. The hearing status of all animals was evaluated with auditory brainstem responses (ABR) evoked by condensation "click" sounds. ABR were recorded both prior to noise exposure and immediately before killing the animal. After death, NO concentration in the cochlear lateral wall was directly measured with an NO/ozone chemiluminescence technique. RESULTS: An approximately 1.7-fold increase in NO concentration was observed immediately postnoise exposure, which persisted for up to 28 days. The threshold of ABR elevation (mean, 30 dB SPL) peaked immediately after cessation of noise exposure and gradually resolved to a PTS (mean, 14.5 dB SPL) 56 days after noise exposure when NO concentration had returned to its prenoise exposure level. CONCLUSION: Noise-induced threshold shift, which resolved to a mild PTS, can be partially attributed to NO elevation in the cochlear lateral wall. Our results revealed a nonlinear correlation between ABR recovery and depletion of NO, indicating that the mechanisms of NO changes in the cochlear lateral wall may be more complicated than previously conceived and that other pathophysiologic mechanisms may also play important roles in noise-induced PTS.