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目的:观察N 甲基 D 天冬氨酸(NMDA)受体的非竞争性拮抗剂MK 801在声损伤中对暂时性阈 移(TTS)或永久性阈移(PTS)的保护作用。方法:将40只豚鼠平均分为两组,分别暴露于倍频程噪声(4kHz中 心频率)110dBSPL3h或115dBSPL5h。取110dB或115dB豚鼠各10只(药物组)在噪声暴露前和后立即 给予MK 801(0.5mg/kg体重,腹腔内注射);另各10只豚鼠(对照组)在相同的时间给予等体积的生理盐水腹腔 内注射。测试暴露前后听性脑干反应(ABR)的阈值,透射电镜观察毛细胞及传入神经末梢的形态。结果:110 dB药物组和对照组动物在噪声暴露后立即测试TTS,两组差异无统计学意义(P>0.05);1周后两组阈移都消 失。115dB药物组暴露后1周阈移明显低于对照组(P<0.05);暴露后3周,该药物组残留的PTS仍显著低于 对照组(P<0.01)。经超微结构检查,110dB药物组和对照组的毛细胞及传入神经末梢正常;115dB药物组内 毛细胞及传入神经末梢结构正常,对照组内毛细胞及传入神经末梢空泡变性。结论:MK 801对TTS缺乏保护, 对PTS有部分的保护作用。这种保护作用须通过预防内毛细胞及传入神经末梢空泡变性来实现。
AIM: To observe the protective effect of MK 801, a non-competitive antagonist of N-methyl D aspartate (NMDA) receptor, on transient threshold (TTS) or permanent threshold shift (PTS) in acoustic injury. METHODS: Forty guinea pigs were equally divided into two groups and exposed to octave noise (4 kHz center frequency) 110 dB SPL3h or 115 dB SPL5h, respectively. Ten (110 g) or 110 dB guinea pigs (drug group) were given MK 801 (0.5 mg / kg body weight, intraperitoneally) before and immediately after noise exposure; the other 10 guinea pigs (control group) were given the same volume at the same time Saline intraperitoneal injection. The threshold of auditory brainstem response (ABR) before and after exposure was measured, and the morphology of hair cells and afferent nerve terminals was observed by transmission electron microscope. Results: The TTS of rats in the 110 dB group and the control group were tested immediately after noise exposure. There was no significant difference between the two groups (P> 0.05). After one week, the threshold shift disappeared. At 1 week after exposure, the threshold shift of 115dB drug group was significantly lower than that of the control group (P <0.05). After 3 weeks of exposure, the residual PTS in the drug group was still significantly lower than that of the control group (P <0.01). The ultrastructural examination showed that the hair cells and afferent nerve endings in the 110 dB drug group and the control group were normal. The structures of the hair cells and afferent nerve endings in the 115 dB drug group were normal, and the degeneration of the hair cells and afferent nerve endings in the control group. CONCLUSION: MK 801 is deficient in TTS protection and partially protects against PTS. This protection must be prevented by degeneration of inner hair cells and afferent endings.