这是一次完全剔除爆震因素的急性声创伤实验研究。各组实验豚鼠均以中心频率1000Hz的(?)频带噪声,声压级为130dB,暴露1h,然后分组分期处死制片和镜检观察。在噪声暴露前和处死制片前各动物均分别作皮层诱发电位测定阈值,以估计听力。结果表明早期(当日)听力损失较重而结构改变较微,晚期(2周后)听力损伤较轻而结构改变较重。内耳声创伤的机理可能有局部机械损伤和代谢改变两方面,早期的表现以机械损伤为主,无爆震因素的急性声创伤,机械损伤轻微,而晚期较明显的结构改变,则可能是局部代谢改变的后果。 This is an acute acoustic trauma experiment that completely eliminates the detonation factor. The guinea pigs in each group were exposed to the frequency band of 1000 Hz with a frequency of 130 dB and were exposed for 1 hour. The cortical evoked potentials were measured before noise exposure and before sacrifice, respectively, to estimate hearing. The results showed that the hearing loss was heavier and the structure changed slightly in the early (the same day), and the hearing loss was lighter and the structure changed heavier in the late stage (after 2 weeks). The mechanism of acoustic trauma in the inner ear may have local mechanical damage and metabolic changes in two aspects. The early manifestations are mechanical injury, acute acoustic trauma without detonation, slight mechanical damage, and the more obvious structural changes in the late stage may be localized The consequences of metabolic changes.