| Project/Area Number |
12671648
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
WADA Tetsuro University of Tsukuba, Institute of Clinical Medicine, Associate Professor, 臨床医学系, 助教授 (10282360)
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| Project Period (FY) |
2000 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2002: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | 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 |
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| Research Abstract |
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 trauma
The 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 trauma
The 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
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