2000 Fiscal Year Final Research Report Summary
Establishment of therapeutic strategy for glaucomatous optic neuropathy
| Project/Area Number |
10671640
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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 |
Ophthalmology
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| Research Institution | Gifu University |
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Principal Investigator |
YAMAMOTO Tetsuya Gifu University School of Medicine, Professor, 医学部, 教授 (50134581)
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| Co-Investigator(Kenkyū-buntansha) |
KAWASE Kazuhide Gifu University School of Medicine, Clinical fellow, 医学部・附属病院, 助手 (40234067)
TANIGUCHI Toru Gifu University School of Medicine, Assistant professor, 医学部・附属病院, 講師 (30179840)
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| Project Period (FY) |
1998 – 2000
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| Keywords | glaucoma / optic neuropathy / neuroprotection / mitomycin C |
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| Research Abstract |
Clinical investigation : Glaucoma filtering surgery with adjunctive mitomycin C was critically evaluated. The surgery was found to have excellent ocular hypotensive effect with preserving the visual field. It, however, caused visual acuity deterioration in a substantial number of cases, mainly by cataract development. A multivariate analysis revealed that vascular compromise such as the presence of disc hemorrhage is a significantly negative prognostic factor for normal-tension glaucoma. Treatment with calcium-blockers as well as carbon dioxide inhalation improved orbital hemodynamics.
New delivery system for mitomycin C : A new delivery system for mitomycin C as an adjunct to glaucoma surgery was investigated. Mitomycin C dissolved in a thermosetting gel clearly improved the surgical success in the rabbit with significant decrease in the total dose of the agent. A nonpenetrating glaucoma surgery with an aid of an excimer laser was investigated and found to be performed easily and quantitatively.
Neuroprotective treatment : We established two new types of rat models for neuroprotective study. Using the models, some drugs such as NMDA receptor antagonists, tacrolimus, betaxolol and so on, were found to have neuroprotective effect against retinal ganglion cell death caused by glaucomatous optic neuropathy.
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