Cochlea protection against acoustic trauma

耳蜗对声损伤的保护

• 批准号: 12671648
• 负责人: WADA Tetsuro
• 金额: $ 2.3万
• 依托单位: University of Tsukuba
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2000
• 资助国家: 日本
• 起止时间: 2000 至 2003
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12671648/
• 关键词: compound action potential; threshold shift; protection of the cochlea; acoustic trauma; transient ischemia; 蝸牛鼓室階カニュレーション; 肝細胞増殖因子

The mechanisms of the cochlea injury are still unclear. Two major factors, ischemiareperfusion injury and acoustic overstimulation, which causes the cochlea injury were investigated to elucidate the similarity and the difference of both injuries. 7-nitroindazole, a relatively selective neuronal nitric oxide synthase (nNOS) inhibitor, was administered and the protective effect was observed against the transient ischemia. The result confirm the involvement of NO and nNOS in the cochlear -injury induced by transient local anoxia. However, NOS inhibitor did not protect the cochlea function against acoustic over-stimulation. The involvement of NO and nNOS was supposed to be less important in the cochlea injury due to the acoustic traumaThe oxygen free radicals were considered to be another mechanism of cochlear injury. The protective effects of glucocorticoids and dehydroepiandrosterone sulfate were confirmed. Although those detailed mechanism was not still determined, the scavenging oxygen free radicals was one of the possibilities. One free radical scavenger was confirmed to have protective effect against acoustic over-stimulation. This result suggested the involvement of oxygen free radicals in the injury induce by acoustic traumaThe differences of the mechanisms of both injuries were revealed by using specific medicines with the injuries. Further study should provide a more precise identification of the basic mechanisms responsible for the injury. These results will lead to new strategies for the protection and the treatment of the cochlea injuries

耳蜗损伤的机制尚不清楚。本研究探讨了引起耳蜗损伤的两个主要因素，即缺血再灌注损伤和声刺激过度，以阐明两者损伤的异同。应用相对选择性的神经型一氧化氮合酶（nNOS）抑制剂7-硝基吲唑（7-nitroindazole），观察其对短暂性脑缺血的保护作用。结果证实NO和nNOS参与了短暂性局部缺氧所致的耳蜗损伤.然而，NOS抑制剂不能保护耳蜗功能免受声过度刺激。NO和nNOS在耳蜗损伤中的作用不明显，氧自由基是耳蜗损伤的另一机制。糖皮质激素和硫酸脱氢表雄酮的保护作用得到证实。虽然这些详细的机制尚未确定，但清除氧自由基是可能的。一种自由基清除剂被证实对声过度刺激具有保护作用。结果提示氧自由基参与了声损伤的发生。进一步的研究应能更准确地查明造成这种伤害的基本机制。这些结果将为耳蜗损伤的保护和治疗提供新的策略

项目成果

Tabuchi K, Tsuji S, Wada T, et al.: "Effect of ketamine, dextromethorphan, and MK-801 on cochlear dysfunction induced by transient ischemia"Annals Otology Rhinology Laryngology. 111. 44-49 (2002)

Tabuchi K、Tsuji S、Wada T 等人：“氯胺酮、右美沙芬和 MK-801 对短暂性缺血引起的耳蜗功能障碍的影响”《Annals Otology Rhinology Laryngology》。

Tabuchi K, Oikawa K, Uemaetomari I, Tsuji S, Wada T, Hara A: "Glucocorticoids and dehydroepiandrosterone sulfate ameliorate ischemia-induced injury of the cochlea"Hearing Research. 180. 51-56 (2003)

Tabuchi K、Oikawa K、Uemaetomari I、Tsuji S、Wada T、Hara A：“糖皮质激素和硫酸脱氢表雄酮可改善缺血引起的耳蜗损伤”听力研究。