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1 General aspects (1)   1.1 Epidemiology (2)   1.2 Population genetics (8)   1.3 Pathogenesis (3)   1.4 Quality of life (5)   1.5 Glaucomas as cause of blindness (4)   1.6 Prevention and screening (4) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (1)   2.2 Cornea (0)   2.3 Sclera (0)   2.4 Anterior chamber angle (0)   2.5 Meshwork (11)     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 (2)   2.9 Ciliary body (4)   2.10 Lens (1)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (2)   2.13 Retina and retinal nerve fibre layer (15)   2.14 Optic disc (12)   2.15 Optic nerve (3)   2.16 Chiasma and retrochiasmal central nervous system (0)   2.17 Stem cells (0)   2.20 Other (1) 3 Laboratory methods (5)   3.1 Microscopy (1)   3.2 Electron microscopy (3)   3.3 Immunohistochemistry (6)   3.4 Molecular genetics (4)     3.4.1 Linkage studies (0)     3.4.2 Gene studies (0)   3.5 Molecular biology incl. 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with intraocular tumors (0)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (0)       9.4.10 Glaucomas associated with hemorrhage (0)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (1)       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 (3)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (2)     9.4.15 Glaucoma in relation to systemic disease (8)     9.4.20 Other (2) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (9) 11 Medical treatment (1)   11.1 General management, indication (4)   11.2 Cholinergic drugs (3)   11.3 Adrenergic drugs (1)     11.3.1 Epinephrine (1)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (10)     11.3.4 Betablocker (14)     11.3.5 Other (0)   11.4 Prostaglandins (31)   11.5 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Without tube implant (5)     12.8.2 With tube implant or other drainage devices (6)     12.8.3 Non-perforating (9)     12.8.4 Using laser (1)     12.8.5 Other (0)     12.8.10 Woundhealing antifibrosis (12)     12.8.11 Complications, endophthalmitis (13)   12.9 Trabeculotomy, goniotomy (1)   12.10 Cyclodestruction (6)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (4)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (0)     12.14.3 Phacoemulsification (5)   12.15 Capsulotomy (0)   12.16 Vitrectomy (0)   12.17 Anesthesia (6)   12.20 Other (2) 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 (3)

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Abstract #6863 Published in IGR 4-1

Potentiation of sympathetic neurotransmission in bovine isolated irides by isoprostanes

Opere CA; Awe SO; Harris LC; Leday AM; Ohia SE
Free Radical Research 2001; 35: 257-264

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Isoprostanes (IsoP) are formed by free radical catalyzed peroxidation of arachidonic acid independent of the cyclooxygenase enzyme. In the present study, the authors examined the effect of IsoP on norepinephrine (NE) release from the bovine isolated iris. Furthermore, they studied the role of IsoPs in hydrogen peroxide (H2O2)-induced enhancement of NE release from this tissue. Isolated bovine irides were prepared for studies of [3H]NE release using the superfusion method. Release of [3H]NE was induced via electrical field stimulation. Both 8-iso-prostaglandin E2 (E2-IsoP) and 8-iso-prostaglandin F2α (F2-IsoP) produced a concentration-related enhancement of field-stimulated [3H]NE release from isolated bovine irides, an effect that was mimicked by the thromboxane (Tx) receptor agonist, U46619 and by H2O2. The Tx-receptor antagonist, SQ 29548 inhibited responses to E2-IsoP (10 μm) with an IC50 of 370 ± 50 nM. SQ 29548 (10 μm) also blocked the enhancement of electrically-evoked [3H]NE release induced by U46619 (10 μm) but not that caused by H2O2 (300 μm). The Tx synthetase inhibitor, carboxyheptylimidazole (10 μm) prevented the stimulatory effect of E2-IsoP on evoked [3H]NE release without affecting responses induced by H2O2. The authors conclude that IsoPs can enhance sympathetic neurotransmission in the bovine isolated iris, an effect that can be blocked by a Tx-receptor antagonist. Furthermore, endogenously produced Tx's mediate the stimulatory effect of IsoPs on NE release. However, endogenously generated IsoPs or Txs are not involved in H2O2-induced potentiation of sympathetic neurotransmission.

Dr. C.A. Opere, Department of Pharmaceutical and Administrative Sciences, School of Pharmacy and Allied Health Professions, Creighton University, 2500 California Plaza, Omaha, NE 68178, USA

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Classification:

11.14 Investigational drugs; pharmacological experiments (Part of: 11 Medical treatment)

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