目的为解决长期监测鸡听觉功能时常用的圆窗膜电极移位的问题，提高测试结果的稳定性，建立了一种新的电极埋植方法－“圆窗埋植电极”（round window implanted electrode）。结合听觉传入神经病变模型评价该方法在实际使用中的稳定性。方法 12只白色Leghorn鸡平分为KA组（经鼓阶灌注kainic acid，选择性地破坏耳蜗传入神经树突）和正常组（不做耳蜗灌注）。暴露鸡的左侧圆窗，在其骨缘内钻孔后植入银球电极。测定电极植入后即刻（给药前）、1天和1、2、4周的听神经复合动作电位（CAP）。结果 同一动物各次CAP波形重复性好，两组动物的振幅、潜伏期和听反应阈均达到满意的稳定性。讨论 与传统的圆窗膜电极比较，圆窗埋植电极植入部位与基底膜的相对位置较恒定；组织愈合后，电极更不会移位，确保了测量数据的稳定性。结论 该方法稳定可靠，改善了振幅的稳定性，使振幅成为听神经动作电位的一项灵敏而可靠的观察指标。本文详细介绍电极安装方法、检测结果，并讨论与CAP记录有关的问题。

目的：观察不同剂量谷氨酸（Glu）类似物海人酸（kainic acid， KA）导致鸡基底乳头（以下称为“耳蜗”）传入神经元迟发性神经元死亡（Delayed neuron death， DND）及相应的耳蜗电生理改变，探讨兴奋性神经元死亡的发生规律。方法：34只成年来亨鸡分3组。第一组经左耳蜗鼓阶灌注高剂量KA（5mM，KA-H组）后测量不同时点的CAP、CM和DPOAE，并观察耳蜗显微和超微结构变化；第二组灌注低剂量KA（0.3mM，KA-L组）后只观察各时点耳蜗形态变化；第三组灌注Hank氏液（HBSS）作对照。结果：① KA灌注后，KA-H和KA-L组高毛细胞（THC）下方的传入树突均迅速水肿，CAP振幅大幅下降；矮毛细胞（SHC）的形态不受影响。② KA灌注后，KA-H组大量传入神经元于2～4周后发生DND并有不可逆听力损伤，但THC长期存活；而KA-L组传入神经元数目无明显减少，且神经元和髓鞘病变在1周后开始恢复。结论：① KA以剂量依赖性方式选择性损伤鸡耳蜗传入神经元；局部高浓度可造成DND，其发生的时间在KA处理2～4周后；② 鸡耳蜗THC可在没有传入突触联系的情况下长期存活，这可能用作实验模型；③ 为推测人类耳蜗兴奋性损伤及其机理，有必要用生理性递质Glu对哺乳动物进行在体实验。

目的：针对鼻窦内窥镜下鼻窦炎性疾病手术后上颌窦口狭窄/闭塞的预防问题，探讨术中人为扩大上颌窦口对术后上颌窦口狭窄/闭塞的影响。方法：对照研究术中不扩大和扩大上颌窦口对术后上颌窦口狭窄/闭塞发生率的影响。试验组50例（85侧）除5侧外，均不扩大上颌窦开口；而对照组50例（92侧）除7侧外，均按常规扩大上颌窦开口。手术半年后根据鼻窦内窥镜检查和临床表现评估上颌窦口的开放程度。结果：试验组的上颌窦口狭窄率为7.06%，对照组17.39%（P<0.05）。结论：除非上颌窦口有不可逆的病变，不要人为地将其扩大，这样更有利于恢复其自然形态和功能。作者还对鼻窦内窥镜手术中上颌窦口的处理方法问题提出了建议。

Kainic acid (KA) is a potent glutamate analog that can temporarily or permanently damage glutamatergic neurons. The purpose of the present study was to determine the short-and long-term effects of KA on chicken otoacoustic emissions and cochlear potentials. A chronic electrode was used to record the compound action potential (CAP), cochlear microphonic (CM), and the slow, positive neural potential (SPNP), a predominantly dc response. The CM, CAP, SPNP, and distortion product otoacoustic emissions (DPOAEs) were recorded before and after infusing 10/A of a low dose (KA-L, 0.3 mM) or high dose (KA-H, 5 mM) of KA into scala tympani. KA caused a rapid and large reduction in CAP and SPNP amplitude in both the KA-H and KA-L groups; however, the CM and DPOAEs were largely unchanged. The amplitude of the CAP and SPNP in the KA-L group began to recover around 1 week post-KA, but was approximately 50% below normal at 4 weeks post-KA. In contrast, the CAP and SPNP showed no signs of recovery in the KA-H group. The results suggest that KA has no effect on the CM and DPOAEs generated by the hair cells, but electively damages the CAP generated by the cochlear ganglion neurons. The reduction in the avian SPNP suggests that the response originates in the cochlear afferent neurons, unlike the summating potential (SP) in mammals that is generated in hair cells. ~ 2000 Acoustical Society of

Kainic acid (KA) selectively damages afferent synapses that innervate, in chickens, mainly tall hair cells. To better understand the nature of KA-induced excitotoxic damage to the cochlear afferent neurons, KA, at two different concentrations (0.3 or 5mM), was injected directly into the inner ear of adult chickens. Pathologic changes in the afferent nerve ending and cell body were evaluated with light and transmission electron microscopy at various time points after KA application. The compound action potential (CAP) and cochlear microphonic (CM) potential were recorded to monitor the physiologic status of the afferent neurons and hair cells, respectively. Hair cell morphology and function were essentially normal after KA treatment. However, afferent synapses beneath tall hair cells were swollen within 30 minutes after KA at both low (KA-L) and high (KA-H) doses. In the KA-L group, the swelling disappeared within 1 day and the morphology of the postsynaptic region returned to near normal condition. In the KA-H group, by contrast, the vacant region beneath tall hair cells remained evident even 20 weeks after KA. The number of cochlear ganglion neurons in the KA-H group decreased progressively from 1 to 8-20 weeks, whereas hair cells in the basilar papilla remained morphologically intact out to 20 weeks after KA. There was no significant change in neuron number in the KA-L group. Temporal changes in the CAP amplitude paralleled the anatomic changes, although the CAP only partially recovered. These results suggest that KA induces partially reversible damage to cochlear afferent neurons with low KA concentration; above this level, KA triggers irreversible, progressive neurodegeneration.