中耳加压治疗膜迷路积水及其机制的研究

Experimental study of the mechanism of hyperbaric therapy on endolymphatic hydrops in guinea pigs

目的探讨中耳加压是否可以抑制豚鼠膜迷路积水,并探究其可能机制。方法将30只豚鼠随机分为3组,每组10只:对照组不做处理;积水组和加压组腹腔注射醋酸去氨加压素1周(4μg/kg·d),制备膜迷路积水模型。且加压组第2、3周放进压力舱行加压治疗。观察3组动物耳蜗形态和功能的变化;用免疫组化方法检测三组豚鼠耳蜗AQP-2的表达。结果①积水组听脑干反应(ABR)听阈值为([58.34±7.79)dB SPL]高于加压组([33.29±3.26)dB SPL]和对照组([20.84±2.13)dB SPL(]P<0.05);②膜迷路积水程度:积水组R值为(0.49±0.11)较加压组(0.36±0.06)膜迷路积水重(P<0.05);对照组无膜迷路积水。③免疫组化实验:AQP-2主要表达在蜗管外侧壁、Corti’s器、螺旋神经节细胞等处,积水组蜗管外侧壁平均灰度值为(134.63±6.64)较对照组(159.36±2.63)、加压组(147.06±4.91)豚鼠AQP-2的表达增加(P<0.05)。结论①中耳加压可显著减轻豚鼠膜迷路积水并改善了耳蜗功能。②中耳加压使膜迷路积水减轻的治疗机制可能与AQP-2的表达下降有关。

【Objective】To investigate the effect of hyperbaric therapy on endolymphatic hydrops in guinea pigs and explore its possible mechanism. 【Methods】Thirty guinea pigs were divided into three groups. The animals in model and hyperbaric group were given deamino-Cys1, D-Arg8d-vasopressin,（dADH） intraperitoneally 4 μg/kg/d in the first week, while those in the control one were given saline intraperitoneally. The hyperbaric group received HBOT in the pressure chamber fin the second, third week. Close observations were made on the morphologic and functional changes in the guinea pig cochleae. The expression of AQP-2 in the inner ears of all guinea pigs was e- valuated.【Results】Average hearing threshold of auditory brainstem response（ABR） in the pressure group [（33.29± 3.26）dB SPL] and in the control group [（20.84±2.13） dB SPL] was lower than that of the study group[（58.34±7.79）dB SPL]（P 0.05）. AQP-2 were found in the cochlear lateral wall, Corti＇s organ, spiral ganglion and endolymphatic sac. The AQP-2 in the cochlear lateral wall and endolymphatic sac was stronger in the inner ears in the model group（134.63±6.64） than that in those hyperbaric group（147.06±4.91） and in the control one（159.36±2.63）.【Conclu- sions】Research findings indicate that hyperbaric therapy can significantly suppress the development of endolym- phatic hydrops and improve cochlear function in guinea pigs. The mechanism of hyperbaric therapy on endolymphat- ic hydrops may correlate to down-regulation of AQP-2.