内耳开窗术对豚鼠耳蜗电图和膜迷路水肿的影响

目的 通过比较耳蜗电图CAP阈值、SP幅度及组织切片,探讨内耳开窗术对豚鼠听力的影响.方法 将听力正常的5只成年豚鼠的双耳进行配对设计.实验耳在耳蜗鼓岬上行内耳开窗,外接注入生理盐水的微泵,在圆窗膜上放置银球记录电极;对照耳只放置记录电极.分别于术后0,2,4,6天记录耳蜗电图的阈值及SP幅度,比较实验耳和对照耳的差异.结果 实验耳和对照耳的耳蜗电图在8 kHz的CAP阈值、SP幅度无统计学差异(P＞0.05),耳蜗组织切片均未见膜迷路水肿.结论 内耳开窗术对豚鼠听力无影响,不会导致膜迷路水肿,可作为内耳给药的有效途径及动物病理模型建立.     

电离辐射对内耳及脑干听觉通路的影响

电离辐射对听觉系统系统的危害越来越引起人们的重视，本文就电离辐射对内耳形态、听觉功能的影响及损伤机理的研究加以综述，为头颈肿瘤放疗时内耳损伤的防治提供依据。     

婴幼儿听觉脑干诱发电位的正常值

目 的探讨0～2岁婴幼儿听觉脑干诱发电位的正常值。方法 采用听觉脑干诱发电位（BAEP）对37例无耳科疾患的听力正常婴幼儿进行检查，测量Ⅰ．Ⅲ．Ⅴ波峰潜伏期和Ⅰ～Ⅲ．Ⅲ～Ⅴ峰间间期。结果 2岁组的各波峰潜伏期较1月龄组明显缩短，呈非常显著性差异（P〈0．001）；而各年龄组的Ⅰ～Ⅲ峰间潜伏期无明显差异（P〉0．05），2岁组的Ⅲ～Ⅴ峰间间期较1月龄组缩短，有显著差异（P〈0．05）。结论 随着年龄的增长，听觉脑干诱发电位的各波峰潜伏期逐渐缩短，但整个听觉通路的发育可能并不是完全平行的。     

实验性喉脑干诱发电位

正常喉部受刺激后可引起反射性的喉内收运动，在吞咽过程中这一生理活动能有效地防止误咽。异常喉反射可造成反射性呼吸暂停、特发性喉痉挛甚至窒息。对上述经喉上和喉返神经传导、脑干为媒体的喉感觉通路的功能研究不仅能深入了解误咽的发生机制，而且有利于了解异常喉反射的原因。运用喉脑干诱发电位对喉反射进行研究是一项新的尝试，目前还停留在动物实验阶段，国内尚未见有报道。本文通过刺激成年兔喉上神经而诱发的脑干电位，分析刺激参数和刺激部位改变对电位潜伏期、阈值及波形的影响，以探讨其应用价值。     

豚鼠耳蜗动作电位脑干及原发听皮层诱发电位三组同线引导

利用计算机信号处理技术，对８只（１６耳）豚鼠行耳蜗动作电位、脑干及原发听皮层三组诱发电位同线引导，可根据需要将电位曲线分若干段进行分析，得出ＡＢＣ三组电位正常时域与频域。结果提示，ＡＢＣ三组电位同线记录，既可以分析耳蜗动作电位、脑干电位以及皮层电位的各自特征，同时又可把三组电位作为一个整体，进行宏观分析。     

儿童孤独症患者脑干听觉诱发电位改变的初步观察

目的：通过观察儿童孤独症患者患者脑干听觉诱发电位的改变,探讨听觉诱发电位检测在听觉障碍儿童孤独症诊断中的临床意义。方法：按DSM－IV诊断标准确诊的15例孤独症患儿的14例正常对照组,同期接受听觉诱发反应检测,比较两组间波Ⅰ-Ⅴ各波峰潜伏期,波峰潜伏期差和波幅的差异。结果：孤独症患儿左侧波Ⅴ、右侧波Ⅱ峰间潜伏期和右侧Ⅰ－Ⅲ、Ⅰ－Ⅴ峰间潜伏期差较对照组显著延长（P＜0．05－0．005）,孤独症组右侧波Ⅲ振幅较对照组增高（P＜0．05）,其他各指标两组间无显著性差异,结论：孤独症患儿脑干听觉诱发电位的突出改变是潜伏期有延长的趋势,对就诊于耳鼻咽喉科的听阈正常而有听觉障碍,言语交往能力着,脑干听觉诱发电位检查潜伏期延长的儿童,应警惕孤独症或其他神经精神发育障碍。     

Ramsay Hunt综合征的听性脑干诱发电位分析

目的:探讨RamsayHunt综合征患者听性脑干诱发电位(ABR)改变。方法:对36例单侧发病,对侧耳正常的RamsayHunt综合征患者进行纯音测试及ABR检查。以健侧耳为对照,分析双耳Ⅰ、Ⅲ、Ⅴ波潜伏期及Ⅰ～Ⅲ、Ⅰ～Ⅴ、Ⅲ～Ⅴ间期的差异。结果:RamsayHunt综合征患者的患侧耳Ⅲ、Ⅴ波潜伏期及Ⅰ～Ⅲ、Ⅰ～Ⅴ间期较健侧耳延长,其差异有统计学意义(P<0.05)。结论:RamsayHunt综合征患者常存在听觉通路损害,表现为蜗性损害、蜗后损害或蜗性损害并发蜗后损害,单纯蜗性损害较少见。     

Effect of glycerol on inner ear fluid electrolytes and osmolalities in guinea pigs

Endolymph of the scala media (SM) and perilymph of the scala vestibuli (SV) and scala tympani (ST) were collected from the basal turn of anesthetized guinea pigs before and after intravenous administration of glycerol (3 g/kg). Sound-evoked responses were recorded during the test periods. Blood, CSF, and perilymph of the ST were also collected continuously after the injection. The osmolalities and chloride concentrations of the collected samples were determined. In another experiment, the continuous changes of potassium and chloride concentrations in endolymph and perilymph of the ST before and after the injection were measured by ion-selective electrodes. The osmolalities in CSF and perilymph lagged behind the increase in serum osmolality. The osmolalities in endolymph and perilymph increased gradually after the injection, reached maximum values after 90 minutes, and then decreased. The changes in chloride and potassium concentrations in endolymph and perilymph had similar tendencies. But the increases in chloride concentrations in perilymph of the SV and ST were much less than that in endolymph. We propose that most of the osmolality increase in perilymph is due to glycerol or other osmotically active substances and that the osmolality increase in endolymph is due to water shift.     

Effect of inner ear immune response on the caloric nystagmus in guinea pigs

The effect of direct antigen (KLH) challenge of endolymphatic sac (e. sac) on caloric response was investigated in guinea pigs. The caloric response was not significantly suppressed both in the primary KLH challenged ears and in the PBS challenged ears as compared to the unchallenged contralateral ears. In the animal of secondary KLH challenge of the e. sac, the caloric response was significantly reduced in the challenged ears as compared to the unchallenged contralateral ears and to the PBS challenged ears. These result suggested that local immune reaction mounted in the e. sac caused immune injury not only to the e. sac but also to the vestibular function.     

Effect of inner ear immune response on vestibular function in guinea pigs]

We examined vestibular dysfunction and histological damage caused by direct antigen challenge to the endolymphatic sac in guinea pigs. We observed spontaneous nystagmus every eight hours and performed caloric testing every week following endolymphatic sac secondary KLH challenge. Spontaneous nystagmus was seen in 12 of 18 animals, and nystagmus in all directed toward the unchallenged ear (paralytic). The caloric response time courses were classified into two types, which were irreversible type and reversible type after endolymphatic sac KLH challenge. The immune injury of animals with irreversible type was thought to be stronger than that of these with reversible type. The spontaneous nystagmus of irreversible type animals was longer than that of reversible type animals. The temporary vestibular dysfunction was thought to be similar to that observed in Meniere's disease.     

Otoconin 90蛋白在豚鼠内耳的表达

目的观察Otoconin 90蛋白在内耳的表达情况,探讨其在耳石代谢中的意义。方法采用免疫组织化学SP方法 (streptavidin-perosidase,链霉菌抗生物素蛋白-过氧化物酶连结法)检测正常豚鼠内耳切片各主要部位Otoconin 90表达情况。结果 Otoconin 90蛋白不只在椭圆囊和球囊囊斑的感觉上皮有表达,在与其临近和相对位置的非感觉上皮,以及壶腹、半规管和耳蜗等多个部位均有丰富表达,在椭圆囊和球囊囊腔、半规管内等也有染色阳性物质出现。结论 Otoconin 90蛋白在内耳呈现出"多点"表达的特点,提示内耳多处产生Otoconin 90,可能最后转运至椭圆囊和球囊囊斑,在此与钙离子相互作用形成耳石。     

Effect of peroral glycerol administration on inner ear fluid electrolytes of guinea pigs

After the oral administration of 50% glycerol (12 mL/kg), serum, CSF and inner ear fluids from scala tympani perilymph, scala vestibuli perilymph, and scala media endolymph were collected from normal guinea pigs under sodium pentobarbital anesthesia (25-35 mg/kg). The sodium and potassium concentrations were determined by microflame photometry. Increases in sodium concentrations were found in CSF, scala tympani perilymph, scala vestibuli perilymph, and cochlear endolymph. No significant change was observed in the serum. These sodium increases were considered to be due to the dehydration caused by the osmotic action of glycerol. Potassium concentration was increased only in scala tympani perilymph. Oral administration of glycerol was found to be more gradual and effective in dehydration compared to intravenous injection.     

泊洛沙姆407局部灌注对豚鼠中耳及内耳的影响

目的观察泊洛沙姆407在豚鼠体内的生物降解与排出过程，以及对听泡结构及功能的影响。方法10只健康豚鼠右侧圆窗龛灌注100μl 20％泊洛沙姆407原位凝胶作为实验组，左侧灌注生理盐水作为对照组，另取2只豚鼠不予处理作为阴性对照。灌注前及灌注后第3、7、14、28及49天行听性脑干反应（auditory brainstem response，ABR）检测，每次检测后处死2只动物，取出听泡，固定，石蜡包埋连续切片，观察凝胶在中耳腔内的生物降解情况以及对中耳腔黏膜、圆窗膜、耳蜗和前庭终器结构的影响。结果圆窗龛灌注泊洛沙姆407凝胶后ABR阈值较灌注前有所提高，但在第49天恢复至灌注前水平。第49天时凝胶基本完全降解或排出，光镜下残留少量絮状物，内含少量炎性细胞。凝胶灌注对中耳腔黏膜、圆窗膜、耳蜗及前庭终器结构均无明显影响。结论泊洛沙姆407凝胶在听泡内通过生物降解和经咽鼓管排出两种形式清除，对听泡组织无明显致炎作用，对ABR阈值有暂时性影响，但未见耳蜗及前庭终器功能和结构有不可逆性损伤。     

Noise-induced inner ear damage in newborn and adult guinea pigs

Two-day (Group A), eight-day (Group B), and eight-month (Group C) old guinea pigs were exposed to 30 continuous hours of white noise at 119–120 db SPL. One month later pathology of the organ of Corti was evaluated and quantitated by use of the surface preparation technique. Percent cell damage was determined for outer hair, inner hair, outer pillar, and inner pillar cells at each of the four turns of the cochlea and for the cochlea as a whole. Comparisons of pathology of each cell type were made between groups. Mean percent outer hair cell damage per cochlea (± 1 S.E.) was 23.72 ± 3.69 for Group A, 36.98 ± 5.76 for Group B, and 7.24 ± 1.75 for Group C. There was no significant difference in outer hair cell damage between Groups A and B. Outer hair cells of Group A were significantly more damaged than those of Group C when damage in the cochlea as a whole was considered due to significantly greater damage in Group A at three and one half turns; likewise, outer hair cells of Group B were significantly more damaged than those of Group C when damage in the cochlea as a whole was considered due to significantly greater damage in Group B at two and one half and at three and one half turns. A similar effect was observed in terms of pathology of inner hair cells and pillar cells: there was a trend toward increased damage in animals of Groups A and B compared with C. Group C showed no outer or inner pillar cell damage, and only one of six animals had alterations in inner hair cells. In contrast, outer and inner pillar cells were damaged in Groups A and B, and four of six animals of Group A and six of eight of Group B showed inner hair cell damage. Recent electrophysiological and audiometric studies are discussed which, with the results of the present study, indicate greater susceptibility of young cochleas when compared with older cochleas, to noise-induced physiological and pathological alterations. It would seem medically prudent to take special precautions to avoid exposing newborns to excessive noise.     

The histologic study of the inner ear in guinea pigs on anaphylatoxin

Complement is known to relate to many inflammatory reactions. C4a, C3a and C5a, known as anaphylatoxins, are known to cause strong inflammatory reactions. In this study, the role of anaphylatoxins on the pathogenesis in the cochlea was examined. On hundred forty six male Harley guinea pigs, weighing about 350 grs, all susceptible to preyer's reflex, were used in this study. Anaphylatoxins were made from guinea pig serum treated with zymosan, and inoculated into the carotid artery of the guinea pigs. Parts of these animals were sacrificed and examined at ten minutes, one day, two days, three days, seven days, ten days and fifteen days after injection of anaphylatoxins. Pathological changes in inner ears were observed by light microscopy. After 10 minutes, inner ears were found morphologically normal. After one day, inner ears were found to be almost morphologically normal but the stria vascularis was observed with cystic formation. After two days, cystic formations in the stria vascularis were enlarged and Reissner's membranes were collapsed in some other animals. After three days, the stria vascularis in the various cochlear turns except in the basal turn, were extremely atrophied, some cochlear nerves showed degeneration and some cochlea showed endolymphatic hydrops. After seven days, ten days and fifteen days, the morphological changes showed atrophy in the stria vascularis similar to the results observed on the third days. Atrophy in the stria vascularis was improved gradually with time, but the degeneration of the cochlear nerve was not improved. Opinions have been divided on the cause of inner ear disease including Meniere's disease. Many authors have reported that infectious diseases, for example mumps, measles and cytomegalovirus infection, have caused human sensorineural hearing loss. These diseases have been reported to result in atrophy in the stria vascularis, degeneration of the cochlear nerve and some other pathological changes. In this study, it was clearly observed that the atrophy of the stria vascularis, the endolymphatic hydrops and other morphological changes were caused by introduction of anaphylatoxins. These results were similar to the pathological changes observed in inner ear diseases in human beings. Therefore, inflammatory substances, including anaphylatoxins, were closely related to the cause of inner ear diseases. The animal model used in this report is considered to be important for elucidating the pathogenesis of inner ear diseases.