Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2001
Beta-adrenergic blocker therapy and the trabecular meshwork.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Gottanka J, Johnson D H, Martus P, Lütjen-Drecoll E
Аннотация
PURPOSE: To determine whether beta-adrenergic blocker (beta-blocker) therapy for glaucoma causes changes in the trabecular meshwork due to underperfusion.
METHODS: Thirty-five eyes from 19 donors with primary open-angle glaucoma (POAG) were divided into three groups: eyes receiving beta-blocker therapy along with standard medications, eyes receiving standard medications but no beta-blockers, and eyes with elevated intraocular pressure but receiving no therapy. Transmission electron microscopy was used to assess the extracellular material of the cribriform region, the structure of the trabecular lamellae, and pigmentation of the trabecular cells. Six eyes from four normal donors were used as controls.
RESULTS: No specific changes in the trabecular meshwork were found in eyes receiving beta-blocker therapy. The amount and composition of the extracellular matrix of the cribriform region and the morphology of the lamellae were similar among the three groups of eyes with POAG. Pigmentation of trabecular cells appeared to be a marker for aqueous flow, as significantly more cells contained pigment in regions of the meshwork with thin or normal lamellae than in regions with thickened and fused lamellae. These regions were variable around the circumference of the eye, and were similar between eyes with and without beta-Blocker therapy.
CONCLUSION: beta-Blocker therapy could not be proven to cause underperfusion changes in the trabecular meshwork or other discernible effects. Preferential pathways for aqueous flow probably exist within regions of the trabecular meshwork, as evidenced by lamellar appearance and pigmentation of the adjacent trabecular cells.
METHODS: Thirty-five eyes from 19 donors with primary open-angle glaucoma (POAG) were divided into three groups: eyes receiving beta-blocker therapy along with standard medications, eyes receiving standard medications but no beta-blockers, and eyes with elevated intraocular pressure but receiving no therapy. Transmission electron microscopy was used to assess the extracellular material of the cribriform region, the structure of the trabecular lamellae, and pigmentation of the trabecular cells. Six eyes from four normal donors were used as controls.
RESULTS: No specific changes in the trabecular meshwork were found in eyes receiving beta-blocker therapy. The amount and composition of the extracellular matrix of the cribriform region and the morphology of the lamellae were similar among the three groups of eyes with POAG. Pigmentation of trabecular cells appeared to be a marker for aqueous flow, as significantly more cells contained pigment in regions of the meshwork with thin or normal lamellae than in regions with thickened and fused lamellae. These regions were variable around the circumference of the eye, and were similar between eyes with and without beta-Blocker therapy.
CONCLUSION: beta-Blocker therapy could not be proven to cause underperfusion changes in the trabecular meshwork or other discernible effects. Preferential pathways for aqueous flow probably exist within regions of the trabecular meshwork, as evidenced by lamellar appearance and pigmentation of the adjacent trabecular cells.