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卡那霉素、庆大霉素等抗生素常引起耳聋,目前尚无较好的防治方法。卡那霉素对内耳的毒性作用,主要先影响有关的酶功能,继而破坏毛细胞而致聋。甲状腺激素具有促进蛋白质合成、增强细胞生物氧化的功能。因此可能具有减轻卡那霉素耳毒性的作用。本实验以耳廓反射、内耳生物电及耳蜗铺片为指标,观察甲状腺激素对卡那霉素耳中毒的预防。实验豚鼠分两组,各13只,对照组每天注射卡那霉素300mg/kg,共10天;甲状腺素组先隔天服甲状腺片20mg共四次,以后给予与对照组相同剂量卡那霉素,同时仍隔天服甲状腺片20mg直至停药后16天,前后总共服17次。结果:(1)耳廓反射阈变化,对8、4、2KHz三个频率听力均下降的耳,对照组为11只耳,甲状腺素组为3只耳,两者差异显著。听力下降的频率范围及程度,对照组比甲状腺素组更大。对照组听力下降开始出现的时间明显早于甲状腺素组;(2)内耳生物电,0～80dβ不同程度短声引起的耳蜗微音器电位与听神经动作电位幅值甲状腺素组动物均高于对照组;(8)耳蜗铺片,对照组大部分动物耳蜗各回的毛细胞严重变性缺损,甲状腺素组耳蜗病变仅局限在底回。以上结果表明甲状腺激素能减轻卡那霉素的耳毒性,为耳毒性抗生素致聋的防治提供了一条新的研究途径。
Kanamycin, gentamicin and other antibiotics often cause deafness, there is no better prevention and treatment methods. Kanamycin on the toxic effects of the inner ear, mainly the first to affect the enzyme function, then destroy the hair cells and deafness. Thyroid hormone has the function of promoting protein synthesis and enhancing cell biological oxidation. It may therefore have the effect of reducing kanamycin ototoxicity. In this study, auricle reflex, inner ear bioelectric and cochlear implants as an indicator to observe the prevention of kanamycin ototoxicity of thyroid hormone. The experimental guinea pigs were divided into two groups with 13 rats in each group. The control group was given kanamycin 300mg / kg daily for 10 days. Thyroxine group was given 20mg of thyroid tablets for the next day for 4 times, then the same dose of kanamycin Su, while still taking the next day thyroid tablets 20mg until 16 days after stopping, before and after a total of 17 times. Results: (1) The changes of auricle reflex threshold, hearing loss of the three frequencies of 8,4 and 2 KHz were decreased, the control group was 11 ears, the thyroxine group was 3 ears, the difference was significant. The frequency range and extent of hearing loss were greater in the control group than in the thyroxine group. The onset time of hearing loss in the control group was significantly earlier than that in the thyroxine group. (2) The content of thyroxine in the inner ear bioelectrical system, the amplitude of cochlear microphones caused by 0 ~ 80dβ short-tone and the level of auditory nerve action potential in thyroxine group were higher than those in the control Group; (8) cochlear implants, the control group, most of the animal cochlear hair cells of severe degeneration and degeneration, thyroid hormone group cochlear lesions confined to the bottom. The above results show that thyroid hormone can reduce the ototoxicity of kanamycin and provide a new approach for the prevention and treatment of ototoxicity induced deafness.