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1 General aspects (0)   1.1 Epidemiology (2)   1.2 Population genetics (16)   1.3 Pathogenesis (14)   1.4 Quality of life (1)   1.5 Glaucomas as cause of blindness (1)   1.6 Prevention and screening (0) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (2)   2.2 Cornea (2)   2.3 Sclera (0)   2.4 Anterior chamber angle (0)   2.5 Meshwork (6)     2.5.1 Trabecular meshwork (0)     2.5.2 Schlemms canal (0)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (3)     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 (0)   2.10 Lens (1)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (5)   2.13 Retina and retinal nerve fibre layer (9)   2.14 Optic disc (18)   2.15 Optic nerve (0)   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 (1)   3.2 Electron microscopy (1)   3.3 Immunohistochemistry (0)   3.4 Molecular genetics (1)     3.4.1 Linkage studies (0)     3.4.2 Gene studies (0)   3.5 Molecular biology incl. 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errors in relation to glaucoma (0)   8.1 Myopia (0)   8.2 Hypermetropia (0)   8.3 Contact lenses (0)   8.4 Refractive surgical procedures (0)   8.5 Other (0) 9 Clinical forms of glaucomas (1)   9.1 Developmental glaucomas (3)     9.1.1 Congenital glaucoma, Buphthalmos (4)     9.1.2 Juvenile glaucoma (0)     9.1.3 Syndromes of Axenfeld, Rieger, Peters, aniridia (2)     9.1.4 Other (3)   9.2 Primary open angle glaucomas (0)     9.2.1 Ocular hypertension (0)     9.2.2 Other risk factors for glaucoma (6)     9.2.3 Open angle glaucoma with elevated IOP (0)     9.2.4 Normal pressure glaucoma (14)   9.3 Primary angle closure glaucomas (0)     9.3.1 Acute primary angle closure glaucoma (pupillary block) (6)     9.3.2 Chronic primary angle closure glaucoma (pupillary block) (1)     9.3.3 Plateau iris syndrome (1)     9.3.4 Primary angle closure suspect (0)     9.3.5 Primary angle closure (0)     9.3.10 Other (2)   9.4 Glaucomas associated with other ocular and systemic disorders (0)     9.4.1 Steroid-induced glaucoma (4)     9.4.2 Glaucomas associated with disorders of the cornea, conjunctiva, sclera (0)       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 (1)       9.4.3.1 Pigmentary glaucoma (1)       9.4.3.5 Other (0)     9.4.4 Glaucomas associated with disorders of the lens (0)       9.4.4.1 Exfoliation syndrome (10)       9.4.4.2 Glaucomas associated with cataracts (0)       9.4.4.3 Glaucomas associated with lens dislocation (0)       9.4.4.5 Other (0)     9.4.5 Glaucomas associated with disorders of the retina, choroid and vitreous (1)       9.4.5.1 Neovascular glaucoma (3)       9.4.5.5 Other (1)     9.4.6 Glaucomas associated with inflammation, uveitis (2)     9.4.7 Glaucomas associated with ocular trauma (3)     9.4.8 Glaucomas associated with intraocular tumors (0)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (2)       9.4.10 Glaucomas associated with hemorrhage (0)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (6)       9.4.11.2 Glaucomas in aphakia and pseudophakia (0)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (0)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (1)     9.4.15 Glaucoma in relation to systemic disease (3)     9.4.20 Other (1) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (9) 11 Medical treatment (0)   11.1 General management, indication (11)   11.2 Cholinergic drugs (2)   11.3 Adrenergic drugs (0)     11.3.1 Epinephrine (3)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (5)     11.3.4 Betablocker (13)     11.3.5 Other (0)   11.4 Prostaglandins (20)   11.5 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Without tube implant (9)     12.8.2 With tube implant or other drainage devices (7)     12.8.3 Non-perforating (5)     12.8.4 Using laser (1)     12.8.5 Other (1)     12.8.10 Woundhealing antifibrosis (21)     12.8.11 Complications, endophthalmitis (10)   12.9 Trabeculotomy, goniotomy (5)   12.10 Cyclodestruction (7)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (5)   12.14 Combined cataract extraction and glaucoma surgery (1)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (1)     12.14.3 Phacoemulsification (7)   12.15 Capsulotomy (1)   12.16 Vitrectomy (0)   12.17 Anesthesia (6)   12.20 Other (3) 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 (0) 15 Miscellaneous (5)

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Abstract #5235 Published in IGR 1-2

Ocular hypotensive effect of ramiprilat in chronic and acute models of glaucoma in rabbits

Shah GB; Harma S; Mehta AA; Goyal RK
Indian Journal of Pharmacology 1999; 31: 110-115

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OBJECTIVE: To study the effect of ramiprilat on experimentally induced acute and chronic glaucoma in rabbits. METHODS: Acute glaucoma was produced by i.v. infusion of 5% glucose in rabbits. Injection of alphachymotrypsin into posterior chamber of rabbit eye produced sustained elevation of intraocular pressure (lOP) which lasted for almost 3 months. The effect of ramiprilat(0.1%) and ramipril(0.1%) was studied in these models of glaucoma. The interaction of ramiprilat with acetylcholine was studied on isolated rat ileum. Effect of ramiprilat on the enzyme cholinesterase and angiotensin converting enzyme (ACE) was studied biochemically. RESULTS: Ramiprilat produced significant fall in lOP in normotensive rabbit eyes and also in rabbits with alpha-chymotrypsin induced glaucoma: It prevented the acute rise in lOP due to infusion of 5% glucose. It caused significant potentiation of responses to acetylcholine in isolated rat ileum preparation. True as well as pseudo cholinesterase enzymes of human blood and ACE in aqueous humor were found to be significantly inhibited by ramiprilat. CONCLUSION: Our data suggest a potential ocular hypotensive activity of ramiprilat which may be due to inhibition of ACE (Kininase-II) and cholinesterase.

R.K. Goyal, Department of Pharmacology, L.M. College of Pharmacy, Navrangpura, Ahmedabad-380 009; India

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Classification:

5 Experimental glaucoma; animal models
11.14 Investigational drugs; pharmacological experiments (Part of: 11 Medical treatment)

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