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1 General aspects (0)   1.1 Epidemiology (4)   1.2 Population genetics (10)   1.3 Pathogenesis (13)   1.4 Quality of life (1)   1.5 Glaucomas as cause of blindness (1)   1.6 Prevention and screening (4) 2 Anatomical structures in glaucoma (1)   2.1 Conjunctiva (1)   2.2 Cornea (0)   2.3 Sclera (0)   2.4 Anterior chamber angle (0)   2.5 Meshwork (10)     2.5.1 Trabecular meshwork (0)     2.5.2 Schlemms canal (0)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (5)     2.6.1 Production (0)     2.6.2 Outflow (0)       2.6.2.1 Trabecular meshwork (0)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (0)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (0)   2.9 Ciliary body (2)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (1)   2.13 Retina and retinal nerve fibre layer (11)   2.14 Optic disc (22)   2.15 Optic nerve (1)   2.16 Chiasma and retrochiasmal central nervous system (0)   2.17 Stem cells (0)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (0)   3.2 Electron microscopy (3)   3.3 Immunohistochemistry (3)   3.4 Molecular genetics (2)     3.4.1 Linkage studies (0)     3.4.2 Gene studies (0)   3.5 Molecular biology incl. 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    9.4.1 Steroid-induced glaucoma (4)     9.4.2 Glaucomas associated with disorders of the cornea, conjunctiva, sclera (1)       9.4.2.1 Iridocorneal endothelial syndrome (ICE, incl. irisatrophy) (2)       9.4.2.2 Posterior polymorphous dystrophy (0)       9.4.2.3 Fuchs' endothelial dystrophy (0)       9.4.2.5 Other (0)     9.4.3 Glaucomas associated with disorders of the iris and ciliary body (2)       9.4.3.1 Pigmentary glaucoma (4)       9.4.3.5 Other (1)     9.4.4 Glaucomas associated with disorders of the lens (1)       9.4.4.1 Exfoliation syndrome (9)       9.4.4.2 Glaucomas associated with cataracts (1)       9.4.4.3 Glaucomas associated with lens dislocation (1)       9.4.4.5 Other (0)     9.4.5 Glaucomas associated with disorders of the retina, choroid and vitreous (0)       9.4.5.1 Neovascular glaucoma (5)       9.4.5.5 Other (1)     9.4.6 Glaucomas associated with inflammation, uveitis (5)     9.4.7 Glaucomas associated with ocular trauma (1)     9.4.8 Glaucomas associated 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Without tube implant (8)     12.8.2 With tube implant or other drainage devices (8)     12.8.3 Non-perforating (2)     12.8.4 Using laser (3)     12.8.5 Other (1)     12.8.10 Woundhealing antifibrosis (19)     12.8.11 Complications, endophthalmitis (11)   12.9 Trabeculotomy, goniotomy (4)   12.10 Cyclodestruction (4)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (3)     12.12.3 Phacoemulsification (8)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (1)     12.14.3 Phacoemulsification (8)   12.15 Capsulotomy (0)   12.16 Vitrectomy (2)   12.17 Anesthesia (4)   12.20 Other (7) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (0)   13.2 Outcome (0)     13.2.1 IOP (0)     13.2.2 Visual field (0)       13.2.2.1 Progression (0)       13.2.2.2 Improvement (0)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (1) 15 Miscellaneous (8)

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Abstract #5803 Published in IGR 2-1

Pharmacoydnamics of beta-blocker modulation of aqueous humor production

Rittenhouse KD; Pollack GM
Experimental Eye Research 2000; 70: 429-439

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A conscious rabbit model with microdialysis sampling of endogenous aqueous humor ascorbate was developed in order to assess the pharmacodynamics of beta-blocker modulation of aqueous humor production. CMA/20 microdialysis probes were implanted in the anterior chamber of each eye of rabbits (n=6). After a two-week recovery period, an i.v. bolus of ¹⁴C-ascorbate (20 μCi) was administered. Blood samples and aqueous humor microdialysis probe effluent were collected and analyzed for endogenous and ¹⁴C-ascorbate to estimate the basal rate of ascorbate blood to aqueous humor secretion (Ro). After a one-hour washout, each rabbit received a series of three doses of ³H-propranolol (750-3000 μg, 16.5 μCi mg^-1) every 60 minutes into the lower cul-de-sac of each eye. Probe effluent was analyzed for endogenous ascorbate and ³H-propranolol; ascorbate and propranolol in the iris/ciliary body, vitreous and aqueous was determined at the end of the experiment. Nonlinear least-squares regression analysis of the concentration-time profiles for aqueous humor ascorbate was performed to estimate the change in aqueous humor flow. The average basal aqueous humor ascorbate secretion rate was ~48 μg hr^-1. Propranolol (1500 μg) produced significant increases in aqueous humor ascorbate, this observation is consistent with a reduction in aqueous humor production (~47%). Analysis of intraocular tissue ascorbate indicated that propranolol inhibited ascorbate secretion at the 3000 μg dose, the highest dose examined in this study; this inhibition was not observed at the 750 or 1500 μg doses. Changes in aqueous humor production precipitated by the administration of beta-adrenergic antagonists can be estimated by measuring changes in aqueous humor ascorbate concentrations in the conscious rabbit. Microdialysis sampling of aqueous humor for endogenous ascorbate provides a relevant analytic tool to estimate modulatory effects of anti-glaucoma drugs on aqueous humor production.

Dr. G.M. Pollack, Beard Hall, Campus Box 7360, School of Pharmacy, University of North Carolina, Chapel Hill, NC 27599-7360, USA. email: gary_pollack@unc.edu

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Classification:

11.3.4 Betablocker (Part of: 11 Medical treatment > 11.3 Adrenergic drugs)

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