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Biomechanics of echothiophate-induced anatomic changes in monkey aqueous outflow system

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Abstract

Cynomolgus monkeys underwent long-term topical treatment with echothiophate, echothiophate + atropine, or control solution. Echothiophate-treated eyes exhibited increased intraocular pressure, collapse and densification of the trabecular meshwork with accumulation of extracellular material in the cribriform region, alterations in the shape and orientation of Schlemm's canal and the ciliary muscle, and discontinuity between ciliary muscle bundles and trabecular beams. Atropine or ciliary muscle disinsertion with subsequent scar formation supporting the mesh posteriorly at least partially prevented these alterations. Only sometimes did discontinuing echothiophate treatment restore normal anatomy. Collectively, these findings indicate that the pathophysiology of structural alterations in the outflow apparatus induced by echothiophate (1) is mediated at least in part by an anterior segment muscarinic receptor, (2) involves mechanical factors and underperfusion of the meshwork, and (3) does not involve any direct toxic effect of echothiophate.

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Supported by grant no. 124/2-2 from the Deutsche Forschungsgemeinschaft and by grants EY00137, EY02698 and TW01044 from the National Institutes of Health

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Lütjen-Drecoll, E., Kaufman, P.L. Biomechanics of echothiophate-induced anatomic changes in monkey aqueous outflow system. Graefe's Arch Clin Exp Ophthalmol 224, 564–575 (1986). https://doi.org/10.1007/BF02154746

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  • DOI: https://doi.org/10.1007/BF02154746

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