Seidman M D, Shivapuja B G, Quirk W S
Department of Otolaryngology, Henry Ford Hospital, Detroit, MI 48202.
Otolaryngol Head Neck Surg. 1993 Dec;109(6):1052-6. doi: 10.1177/019459989310900613.
Several studies have demonstrated that noise exposure may result in local vasoconstriction of cochlear vessels. The subsequent decrease in cochlear blood flow may lead to hypoxia and predispose to the formation of free oxygen radicals (FORs). If hypoxia occurs in response to noise exposure, then drugs that scavenge or block the formation of FORs should protect the cochlea from damage resulting from hypoxic or ischemic events as well as noise trauma. Rats were exposed to 60 hours of continuous broad-band noise (90 dB SPL) and treated with superoxide dismutase-polyethylene glycol (SOD-PEG), allopurinol, or a control vehicle. Exposure to noise resulted in significant threshold shifts at each frequency tested (3, 8, 12, and 18 kHz) as measured by tone burst-evoked compound action potentials and cochlear microphonics recorded from the round window. Both of these thresholds in drug-treated animals were attenuated compared with animals exposed to noise alone. These findings show that SOD-PEG and allopurinol may preserve cochlear sensitivity associated with noise exposure. This suggests that noise-induced damage to the cochlea may be related to the activity of FORs.
多项研究表明,噪声暴露可能导致耳蜗血管局部血管收缩。随后耳蜗血流量的减少可能导致缺氧,并易引发游离氧自由基(FORs)的形成。如果因噪声暴露而发生缺氧,那么清除或阻断FORs形成的药物应能保护耳蜗免受缺氧或缺血事件以及噪声创伤造成的损害。将大鼠暴露于60小时的连续宽带噪声(90 dB SPL)中,并用超氧化物歧化酶 - 聚乙二醇(SOD - PEG)、别嘌呤醇或对照载体进行处理。通过从圆窗记录的短纯音诱发复合动作电位和耳蜗微音器电位测量,噪声暴露导致在每个测试频率(3、8、12和18 kHz)出现显著的阈值偏移。与仅暴露于噪声的动物相比,药物处理动物的这两个阈值均有所降低。这些发现表明,SOD - PEG和别嘌呤醇可能保留与噪声暴露相关的耳蜗敏感性。这表明噪声诱导的耳蜗损伤可能与FORs的活性有关。