强短声诱发的清醒豚鼠咬肌肌源性电位

Loud click-evoked masseter myogenic potentials in alert guinea pigs

目的建立强短声诱发的咬肌肌源性电位的豚鼠模型,并确定该电位的起源。方法17只豚鼠随机分成3组,正常对照组5只;5只豚鼠以450 mg/kg剂量每天肌注阿米卡星1次,持续注射18 d,以选择性药物破坏耳蜗;5只豚鼠左侧圆窗区滴注庆大霉素0．05 ml(40 mg/ml)以选择性破坏前庭,另有2只豚鼠左侧圆窗区滴注生理盐水0．05 ml以作为听泡开窗的对照。3组动物分别进行冷热实验、强短声诱发的咬肌肌源性电位以及听性脑干反应(ABR)测试。结果正常对照组豚鼠,120、110、100和90 dB单耳声刺激,单侧记录到的豚鼠咬肌肌源性电位的反应率分别为100%、90%、70%和0%。120、110和100 dB声刺激诱发的肌源性电位的正负波的潜伏期分别为6．73±0．59 ms和8．84±0．56 ms,6．80±0．43 ms和8．92±0．48 ms,以及6．94±0．49 ms和9．00±0．51 ms。平均峰间幅度分别为6．23±2．37μV、6．12±2．24μV和6．36±3．13μV,刺激强度对豚鼠的咬肌肌源性电位的平均潜伏期或峰间幅度无显著影响。采用庆大霉素单侧处理的豚鼠,损伤侧的冷热反应均缺失,而ABR阈值却正常,其损伤同侧声刺激诱发的咬肌肌源性电位缺失。阿米卡星处理组豚鼠冷热实验正常,双侧ABR阈值显著增加,但短声诱发的咬肌肌源性电位均存在。结论豚鼠强短声诱发的咬肌肌源性电位来源于前庭而非耳蜗。

Objective To establish an animal model of loud click-evoked masseter myogenic potential using guinea pigs and to determine the origin of the masseter myogenic potentials. Methods Seventeen guinea pigs were randomly divided into three groups： normal control group （n= 5）, amikacin-administered （AA） group （n= 5） and gentamicin treated （GT） group （n= 7）. In animals of AA group, amikacin was given intramuscularly 450 mg/kg/d for 18 days to destroy cochleae pharmacologically. In animals of GT group, gentamicin 0.05 ml （40 mg/ml） was injected into round window area to destroy vestibule selectively in five animals while saline was injected in two animals serving for control. Each animal of three groups underwent caloric tests and tests for loud click-evoked masseter myogenic potential and acoustic brainstem evoked response （ABR）. Results The response rates for the myogenic potentials on the masseter of guinea pigs in normal control group using 120, 110, 100 and 90 dB monaural acoustic stimulation with unilateral recording were 100%, 90%, 70% and 0% respectively. The mean latencies of the positive and negative peaks for the myogenic potentials elicited by 120, 110 and 100 dB acoustic stimulation were 6.73 ±0.59 and 8. 84±0. 56 ms, 6.80±0.43 and 8.92±0.48 ms, 6.94±0.49 and 9.00±0. 51 ms respectively. The median peak-to-peak amplitudes elicited by 120, 110 and 100 dB acoustic stimulation were 6.23 ±2.37, 6.12 ± 2.24 and 6. 36±3. 13μV respectively. No significant relationship was found between the stimulus intensity and the mean latencies or peak-to-peak amplitude of the masseter myogenic potentials in guinea pigs. For those treated with gentamicin unilaterally, the animals showed absent caloric responses on the lesion side, and absent myogenic potentials on the masseter when using ipsi-lesional acoustic stimulation, while ABR displayed no elevation of the threshold. All AA group animals showed normal caloric responses and loud clickevoked masseter myogenic potentials, although the ABR thresholds were highly elevated. Conclusions Loud click-evoked masseter myogenic potentials recorded on alert guinea pigs are in fact of vestibular origin but not cochlear origin.