窒息对豚鼠耳蜗内直流电位的影响

目的:探讨缺氧引起听功能障碍的发病机制,了解窒息对耳蜗内直流电位(EP)的影响。方法:选择听耳廓反射良好豚鼠,采用血管纹法检测耳蜗内直流电位,观察呼吸暂停时及恢复人工呼吸后耳蜗内直流电位的变化。结果:①正常EP初始值实验组为(76.4±8.4)mV,对照组为(80.8±8.4)mV,组间差异无统计学意义;②呼吸暂停时全部豚鼠经过8~34 s潜伏期后EP迅速下降,EP下降速度与潜伏期呈正相关;③呼吸暂停3 min后EP最低值平均为(-17.5±4.4)mV,与潜伏期及下降速度呈正相关;④恢复人工呼吸后平均(85.0±16.0)s EP恢复至初始值,并有7例出现过冲现象。结论:EP下降预示呼吸暂停时毛细胞生存环境出现异常;呼吸停止3min全部豚鼠EP变为负值,提示呼吸停止3 min不会导致全部毛细胞功能丧失、血管纹也不会发生不可逆功能障碍。     

花椒超临界萃取物对豚鼠离体气管活动的影响

目的探讨花椒超临界萃取物（HJ）对豚鼠离体气管的作用及其机制。方法通过HJ对正常气管、乙酰胆碱（Ach）所致气管痉挛及磷酸组胺（HIS）致气管依内、外钙两种收缩的影响，初步探讨HJ对离体气管的作用及其机制。结果HJ对正常气管、Ach和HIS所致气管痉挛及HIS致气管依外钙收缩有明显的抑制作用，并呈剂量依赖性。结论HJ有平喘的作用。     

豚鼠内耳磁微粒栓塞缺血模型初探

目的　建立豚鼠内耳磁微粒栓塞缺血模型。方法　颈静脉注射羰基铁微粒混悬液(1% ,1ml/kg) ,外耳道置磁铁 ,以诱导磁微粒定向积聚 ,阻塞内耳微血管 ,形成内耳缺血模型。铺片观察膜迷路微血管内磁微粒的分布及变化 ,并计数不同时相点纹血管内红细胞 ;激光多普勒血流仪(laserDopplerflowmetry ,LDF)动态测量耳蜗血流量 (cochlearbloodflow ,CBF)的消长 ;硝酸银染色基底膜铺片计数听毛细胞 ;颞骨切片观察组织病理变化。结果　造模后 1d内耳微血管内出现磁栓 ,2d减少 ,4d基本消失 ;纹血管内红细胞数在造模后 1、2d减少 ,4d基本恢复 ;造模后CBF随即平均 ( x±s,下同 )下降至 5 0 %± 10 % ,维持 2 4h ,2d恢复至 79%± 4 0 % ,4d恢复至 99%± 4 1% ;造模后 1d模型耳听毛细胞无明显异常 ,而 8d外毛细胞纤毛散在缺失 ;切片显示血管纹肿胀变性。结论　磁微粒栓塞成功地造成了豚鼠内耳缺血 ,方法简便 ,易于实施 ,CBF具有可逆性特点 ,可作为内耳缺血性疾病研究及治疗药物筛选的实验模型     

脑源性神经营养因子对耳蜗螺旋神经节的保护作用

目的　观察腺病毒携带的脑源性神经营养因子 (brainderivedneurotrophicfactor,BDNF)在豚鼠耳蜗中的表达 ,及噪声损伤后对螺旋神经节的保护作用。方法　 2 7只白色纯种豚鼠 ,暴露于135dBSPL ,4kHz的窄带噪声 4h。 7d后 ,12只经圆窗注入腺病毒携带BDNF(adenoviral mediatedBDNF ,ad BDNF) ,12只经圆窗注入ad LacZ ,3只注入人工外淋巴液。分别于 1、4、8周后取材 ,石蜡包埋中轴切片后 ,用免疫组化方法 (ABC法 )检测BDNF的表达。于光镜下计数螺旋神经节细胞。结果　在耳蜗各回中BDNF均有表达 ,4、8周组动物较 1周组动物表达弱。在 8周 ,注入ad BDNF组较ad LacZ组和人工外淋巴组螺旋神经节发生退行性病变的数目少 ,螺旋神经节细胞计数结果经统计学t检验 ,P <0 0 1,差异有显著性。结论　腺病毒携带的神经营养因子在耳蜗中能高效表达 ,在噪声损伤情况下腺病毒携带的脑源性神经营养因子对螺旋神经节有保护作用。该研究为基因治疗感音神经性聋提供了坚实的实验基础     

豚鼠耳蜗毛细胞暴露非聚焦超声后的酶组织化学观察

目的　探讨非聚焦超声 (non focusedultrasound ,NFU)对耳蜗毛细胞的影响。方法　以A型超声波诊断仪为超声发射器 ,分别以 2 5MHz、8MHz照射各 15耳豚鼠耳蜗 6h后 30min和 8h行耳蜗基底膜毛细胞铺片及冰冻切片观察琥珀酸脱氢酶 (succinatedehydrogenase ,SDH)组织化学变化。结果　 2 5MHz、8MHzNFU照射豚鼠耳蜗 6h后 8h能引起不同节段基底膜毛细胞SDH酶活性降低 ,其中外毛细胞较内毛细胞SDH酶活性降低更甚。照射后 8h组较照射后 30min组SDH酶活性有明显恢复。结论不同频率NFU超声照射耳蜗达一定剂量可以引起不同部位基底膜毛细胞的病理性缺氧改变 ,而这种缺氧病理改变在一定暴露剂量下是可逆或部分可逆的。提示耳蜗毛细胞可能与超声感受有关 ,其中外毛细胞可能起更为重要的作用 ,且不同部位毛细胞与超声感受的频率选择性可能有一定关系     

小青龙汤对哮喘豚鼠肺及胸腺的神经生长因子表达作用研究

目的 探讨小青龙汤时哮喘豚鼠肺及胸腺的神经生长因子(NGF)表达的影响.方法 采用免疫组织化学和RT-PCR法.观察正常对照组、哮喘组、小青龙汤组、氨茶碱组及小青龙汤组配氨荼碱组的豚鼠肺和胸腺NGF表达的变化.结果 哮喘组豚鼠NGF在肺和胸腺表达明显高于正常组,差异具有统计学意义(P相似文献   

针刺及川芎嗪对急性药物性聋豚鼠耳蜗生长相关蛋白GAP-43表达的影响

[目的]探讨川芎嗪、针刺单独应用及联合使用对GM(庆大霉素)致聋豚鼠耳蜗生长相关蛋白GAP-43表达的影响.[方法]将50只豚鼠随机分为5组,即:正常组、模型对照组、TMP(川芎嗪)治疗组、针刺组和TMP加针刺组,每组动物各10只,造模14天[1].即正常组每日按2.5ml/kg剂量腹腔注射生理盐水,其余各组每天腹腔注射庆大霉素100mg/kg,连续14天;同时根据组别的不同立即灌服TMP和(或)针刺相应穴位.造模结束后,豚鼠迅速断头处死,取耳蜗标本.观察指标:TUNEL染色的GAP-43的阳性率和电镜下耳蜗螺旋神经节细胞内GAP-43表达分布情况.[结果]GAP-43在实验动物耳蜗螺旋神经节细胞中都有一定的表达.正常组在胞浆和轴突内表达较弱较少,以轴突表达为主;其它各组表达较其均明显增多,以胞浆表达为主,且均较模型组为多(P<0.05).治疗组中尤以TMP加针刺组表达增多明显,组间显著性差异P<0.05.[结论]针药结合治疗增加GM致聋豚鼠耳蜗GAP-43表达,说明促进GAP-43的表达,可能是中医药防治急性药物性聋的作用原理之一.     

Maturation of auditory evoked potentials in young guinea pigs with binaural conductive hearing loss

Summary A reversible conductive hearing loss produced during the first 4 weeks post partum caused marked alterations in the development of click-evoked auditory brainstem (ABR) and middle latency (MLR) responses in guinea pigs. The early component PI in the ABR in controls showed adult-like latencies at the time of birth, while the later ABR components P_III and P_V and all components investigated in the MLR showed postnatal development characterized by a shortened latency that persisted for the whole period of investigation. The course of the ABR latencies showed the sharpest decrease during the first 2–3 weeks of life, while that for the MLR took place during the first 5 weeks. In addition to the increased ABR thresholds and lengthened ABR latencies due to the conductive hearing loss, development of the ABR inter-peak latencies (IPL) and MLR latencies was retarded. The IPL reached control values 1 week after the end of the deprivation phase, while the delay in MLR started later (4th week) and lasted longer than did that in the ABR. These findings showed that a long-lasting postnatal conductive hearing loss does not generate sustained impairment at the level of the brainstem but can evoke longer-lasting deficiencies at higher stations of the auditory pathway.     

洗必泰的耳蜗毒性实验研究

将２５只豚鼠随机分为０．５％洗必泰１、２、３周组和０．１％洗必泰１周组，７０％酒精（溶剂）１周组。经听泡一次给药（洗必泰），通过耳蜗神经动作电位（ＡＰ）测试及扫描电镜观察，表明洗必泰具有明显耳毒性，与药物浓度及动物存活时间呈正相关。     

Late respiratory response and associated eosinophilic inflammation induced by repeated exposure to toluene diisocyanate in guinea pigs

OBJECTIVE: The study was designed to establish an animal model of toluene diisocyanate (TDI)–induced late respiratory response and to investigate airway inflammatory cell dynamics in this model. METHODS: Guinea pigs were exposed to 2,4-TDI dissolved in ethyl acetate by nasal application according to three schedules. Schedule 1 consisted of sensitization and multiple challenge (n = 58): 10% TDI was applied once daily for 7 days (sensitization) followed by challenges with 5% TDI once weekly for 4 weeks. Schedule 2 consisted of sensitization only (n = 5): 10% TDI was applied once daily for 7 days. Schedule 3 consisted of single challenge only (n = 12): 5% TDI was applied only once. As controls, ethyl acetate was applied according to the three schedules described above. Each animal was premedicated with metyrapone before each challenge. Bronchoalveolar lavage and histologic examination were performed at various times after the last challenge. RESULTS: Schedule 1 induced immediate and late respiratory responses at a prevalence of 63% and 56%, respectively. Schedules 2 and 3 induced an immediate response in some animals but no late response. Neither immediate nor late response was observed in control animals. All of the subgroups of schedule 1 that developed late responses (examined at 2, 3, 6, 24 and 168 hours) showed a significant increase of eosinophils in bronchoalveolar lavage fluid and tissue compared with the corresponding control of each (examined at the same time points). Two of the subgroups with late responses (examined at 3 and 6 hours) were compared with their corresponding subgroups, which were given the same treatment, failed to develop late response, and were examined at the same time points; they again proved to have a significant increase of eosinophils in both samples. Subgroups of schedule 1 without late response (30 minutes, 3 and 6 hours), schedule 2 (6 hours), or schedule 3 (2 and 6 hours) did not show significant changes in lavage or tissue cell composition, except for the schedule 1 subgroup examined at 6 hours, which showed a significant increase of eosinophils only in the tissue compared with its control. CONCLUSIONS: Sensitization and multiple challenge with TDI induced immediate and/or late respiratory responses at a high prevalence in guinea pigs. Eosinophilic but not neutrophilic inflammation was involved in the late response. (J ALLERGY CLIN IMMUNOL 1996;97:1308-19.)