Kumagai M
Department of Otolaryngology, Hokkaido University School of Medicine, Sapporo, Japan.
Hokkaido Igaku Zasshi. 1992 Mar;67(2):216-33.
It is not yet well understood how aspirin acts on the auditory system. This study was aimed at elucidating the effects of aspirin on the cochlear hair cells and cochlear nerve of guinea pigs by recording (1) spontaneous activity of cochlear nerve fibers, (2) compound action potentials (CAPs) evoked by electrical pulses applied to the cochlea through the round window membrane, (3) acoustically evoked action potentials (APs) through the round window membrane and (4) acoustic emissions (sound pressure near the tympanic membrane) evoked by electrical pulses applied to the cochlea. The following results were obtained. (1) After guinea pigs were given aspirin (200 mg/kg) intravenously, a transient reduction in spontaneous activity of cochlear nerve fibers and elevation over the subsequent 10-20 minutes were observed in three of four fibers recorded for more than 30 minutes. The mean spontaneous discharge rate in 102 fibers after aspirin administration (200 mg/kg) was not significantly higher than the control values from 30 to 120 minutes after aspirin administration, while the rate in 112 fibers after aspirin administration (400 mg/kg) was significantly higher. (2) After injecting of 100 mg/kg, 200 mg/kg and 400 mg/kg of aspirin, the amplitude of electrically evoked CAPs decreased significantly, while their latency increased significantly only after injection of 400 mg/kg of aspirin. (3) Changes in the amplitude of acoustically evoked APs and electrically evoked CAPs were compared before and after intravenous injections of 400 mg/kg of aspirin. The AP suppression ratio at low sound intensity was significantly greater than that of CAPs at low and high current levels. (4) After injection of 400 mg/kg of aspirin, the waves of electrically evoked acoustic emissions and their peaks in the frequency analysis disappeared either reversibly or irreversibly. The observed changes in spontaneous activity of cochlear nerve fibers in response to aspirin administration to guinea pigs may represent a tinnitus-like phenomenon. The detection of electrically evoked CAPs suggests that aspirin acts on the cochlear nerve and causes a decrease in its excitability, and the discovery of acoustically evoked APs and electrically evoked acoustic emissions is interpreted as indicating that aspirin acts not only on the cochlear nerve but also on cochlear hair cells.
阿司匹林如何作用于听觉系统尚未完全清楚。本研究旨在通过记录(1)耳蜗神经纤维的自发放电活动、(2)经圆窗膜向耳蜗施加电脉冲诱发的复合动作电位(CAPs)、(3)经圆窗膜记录的声诱发动作电位(APs)以及(4)向耳蜗施加电脉冲诱发的声发射(鼓膜附近的声压),来阐明阿司匹林对豚鼠耳蜗毛细胞和耳蜗神经的影响。获得了以下结果。(1)给豚鼠静脉注射阿司匹林(200mg/kg)后,在记录时间超过30分钟的4根纤维中的3根中,观察到耳蜗神经纤维自发放电活动短暂降低,并在随后的10 - 20分钟内升高。阿司匹林给药(200mg/kg)后102根纤维的平均自发放电率在给药后30至120分钟内不显著高于对照值,而阿司匹林给药(400mg/kg)后112根纤维的放电率显著更高。(2)注射100mg/kg、200mg/kg和400mg/kg的阿司匹林后,电诱发CAPs的幅度显著降低,而仅在注射400mg/kg阿司匹林后其潜伏期显著增加。(3)比较了静脉注射400mg/kg阿司匹林前后声诱发APs和电诱发CAPs幅度的变化。低声强下的AP抑制率显著高于低电流和高电流水平下的CAP抑制率。(4)注射400mg/kg阿司匹林后,电诱发声发射的波及其频率分析中的峰值可逆或不可逆地消失。观察到的豚鼠服用阿司匹林后耳蜗神经纤维自发放电活动的变化可能代表一种耳鸣样现象。电诱发CAPs的检测表明阿司匹林作用于耳蜗神经并导致其兴奋性降低,而声诱发APs和电诱发声发射的发现被解释为表明阿司匹林不仅作用于耳蜗神经,还作用于耳蜗毛细胞。