Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1996: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1995: ¥3,900,000 (Direct Cost: ¥3,900,000)
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Research Abstract |
A quantitative index of tissue blood flow velocity and blood flow measured by laser speckle method (NB) in the optic nerve head (NB_<ONH>) and choroid (NB_<CH>) were determined in experimental animals and normal human volunteers before and after administration of several antiglaucoma drugs which have been clinically used or were under development. Animal study : In albino rabbits, effects of twice daily 2-3 week instillation of 0.5% betaxolol, a beta-1 blocker, 0.5% timolol, a beta-1,2 blocker, 2% carteolol, a beta-1,2 blocker with intrinsic sympathomimetic activity, 0.25% nipradilol, a beta-1,2 blocker alpha-1 blocking activity, and 0.05% bunazosin, an alpha-1 blocker, were studied. Topical unilateral carteolol increased NB_<ONH> in both eyes, while topical unilateral timolol, betaxolol and nipradilol increased it only in ipsilateral eye. Topical unilateral bunazosin showed no effect in both eyes. Intravenous injection of a calcium antagonist, nilvadipine, nicardipine or semothiazil, increased NB_<CH>, while NB_<ONH> was increased only by nilvadipine. To carry out experiments in monkeys, specially disigned monkey chair was first constructed. In experimental glaucoma monkey eyes, oral planidipine, another calsium antagonist, however, showed no significant effect on NB_<ONH>. Human study : Twice daily 3-week unilateral instillation of 0.5% carteolol slightly increased NB_<ONH> in both eyes, while that of 0.5% betaxolol slightly increased it only in ipsilateral eye and that of 0.5% timolol showed no effect in both eyes. Oral nilvadipine, but not semothiazil, increased in NB_<ONH> humans. These results indicate that some beta-blockers can affect optic nerve head circulation when given topically and that some calcium antagonist can increase optic nerve head blood flow, which may have implications in treating glaucoma or in studying pathogenesis of glaucoma.
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