补肾聪耳片对卡那霉素致聋豚鼠听毛细胞修复研究

目的 :探讨补肾聪耳片对卡那霉素致豚鼠感音性神经性耳聋的修复和保护作用。方法 :卡那霉素致聋制作动物实验模型 ,用中药制剂补肾聪耳片进行干预 ,通过听力和耳蜗病理实验观察其改善听力和对耳蜗毛细胞的修复作用。结果 :正常对照组和实验组相比各项观察指标 (耳廓听域反射、听性脑干诱发电位、外毛细胞听毛缺失率差别均有统计学意义 (P<0 01) ,超微结构检查发现中药制剂对耳蜗结构有明显的改善。结论 :补肾聪耳片能恢复神经反射的功能 ,改善耳听力 ,促进毛细胞修复。     

POSSIBLE EFFECTS OF KANAMYCIN AND INCUBATION IN NEWBORN CHILDREN WITH LOW BIRTH WEIGHT

ABSTRACT: In an acoustico-vestibular follow-up investigation of 91 four- to six-year-old children with birth weight below 2 000 g, the same incidence of sensorineural hearing loss (19 %) was found in 54 children treated with kanamycin in the neonatal period as in a group of 37 infants not treated with kanamycin. When comparing a group of children treated with both kanamycin and incubator (54 children) with a group treated with incubator only (16 children), no definite signs of synergism between incubator noise and kanamycin were found. However, the 5 cases of moderate or severe hearing loss all belonged to the group treated with both incubator and kanamycin. These 5 children had more severe neonatal complications, especially apnea, cyanotic spells and hyperbilirubinemia, which may increase the severity of the hearing loss.
Among 56 incubator treated children with normal hearing (ISO standards) 52% had an audiogram pattern suggesting minor noise-provoked cochlear lesions. Among 18 non-incubator treated children with normal hearing only one child (6%) had a similar pattern. It should be stressed, however, that these children had no clinical symptoms of hearing loss.     

磷霉素在减轻卡那霉素耳毒中的作用

为研究磷霉素减轻卡那霉素耳毒的作用机理,我们选用了50只健康豚鼠分两组进行实验,对照组用卡那霉素400mg·kg~(-1)/d 肌注,连续7天;实验组肌注卡那霉素,用量同对照组,连续7天,第四天起肌注磷霉素300mg.kg~(-1)/d,连续7天。两组豚鼠均行 ABR,再用扫描电镜、透射电镜及组织化学反应来检查耳蜗结构.ABR 示自第11天起对照组Ⅳ波消失,而实验组Ⅳ波除1例外均存在,且波形清晰。电镜检查及组织化学反应检查均显示实验组耳蜗外毛细胞损伤明显比对照组耳蜗外毛细胞损伤轻。结果表明,磷霉素可以减轻卡那霉素的耳毒性。     

鼓室内注入催产素对卡那霉素耳毒的拮抗作用

给两组豚鼠肌肉注射卡那霉素(300mg/kg)连续8天,同时由鼓室内分别注入催产紊(10μ/ml)0.12～0.2ml/耳及等量生理盐水。采用耳蜗铺片方法,从形态学方面观察比较了实验组与对照组听毛细胞的损伤程度和范围。结果,两组基底膜各相应回的毛细胞损伤率相比较,使用催产素纽明显低于对照组(P<0.001)。提示鼓室内注入催产素对卡那霉素所致内耳损伤有拮抗作用。     

应用ELISA测定睫状神经营养因子中卡那霉素残留量

目的:建立ELISA检测卡那霉素残留量的方法并进行方法学验证,用于重组技术产品的质量控制。方法:采用间接竞争ELISA方法,样本中残留的卡那霉素将和微孔板上预包被的偶联抗原竞争抗卡那霉素抗体,加入酶标二抗后,用3,3,5,5-四甲基联苯胺(TMB)底物显色,样本吸光值与残留卡那霉素的含量成负相关,用酶标仪进行检测并用SOFT MAX分析软件进行分析。结果:ELISA方法测定卡那霉素残留量在0.5~40.5 ng.mL-1范围内线性良好,且符合四参数方程式:y=(A-D)/[1+(X/C)B]+D,r2≥0.99;板内变异小于15%,板间变异小于20%,实验重复性好,加标回收率在80%~120%之间;该方法检测与庆大霉素、盐酸四环素、链霉素和氨苄西林药物未显示交叉反应。应用该法对1批睫状神经营养因子(CNTF)原液的卡那霉素残留量进行测定,结果表明,每人用剂量CNTF(100μg)卡那霉素残留量小于0.5 ng。结论:该方法具有灵敏度高、操作简便、检测迅速等特点,可用于重组技术产品中卡那霉素残留量的检定。     

卡那霉素在体外对A.healyi的杀伤作用

[目的]观察卡那霉素在体外对棘阿米巴A.healyi的杀伤作用.[方法]用1.0,10.0,100.0g/L卡那霉素和0.2,2.0g/L甲硝唑在体外培养棘阿米巴3,8,24,48h,观察用药前及不同培养时间的生长情况.[结果]1.0g/L卡那霉素对棘阿米巴无抑制作用,10.0g/L卡那霉素在培养48h时及100.0g/L卡那霉素培养24h时抑制棘阿米巴生长,100.0g/L卡那霉素在培养48h时杀伤棘阿米巴.2.0g/L甲硝唑作用48h时仍无明显的杀伤作用.[结论]在体外卡那霉素质量浓度为10.0g/L时对棘阿米巴有抑制作用,100.0g/L时具有杀伤作用.     

Antagonistic Effect of Poria Cocos on Ototoxicity of Kanamycin in Guinea－Pigs

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Serotonin Deficiency Is Associated With Delayed Gastric Emptying

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Effect of Ligustrazine on Kanamycin Ototoxicity

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Damage to sensory hairs of inner hair cells after exposure to noise in rabbits without outer hair cells

We investigated if the noise-induced damage to the stereocilia of inner hair cells (IHCs) was dependent on the integrity of the outer hair cells (OHCs) in rabbit. Prior to the noise exposure a total loss of OHCs in the basal 1.5 to 2 turns was induced by administration of kanamycin (400 mg/kg for 10 days). This left the IHCs apparently normal as observed in the scanning electron microscope. These animals exhibited a 20-60 dB hearing loss before noise exposure. In spite of this pronounced hearing loss, the fusion and inclination of the IHC stereocilia were extensive in these noise-exposed ears. The stereocilia damage occurred at the same noise exposure and was as prominent or even more pronounced than has been noted in ears exposed to noise only. Under the assumption that kanamycin causes selective destruction of OHCs, the results can be interpreted as evidence that the OHCs facilitate the IHCs at low sound levels without being involved in the process which damages IHC stereocilia at high levels of noise.