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1 General aspects (0)   1.1 Epidemiology (2)   1.2 Population genetics (5)   1.3 Pathogenesis (5)   1.4 Quality of life (2)   1.5 Glaucomas as cause of blindness (3)   1.6 Prevention and screening (3) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (2)   2.2 Cornea (6)   2.3 Sclera (1)   2.4 Anterior chamber angle (0)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (7)     2.5.2 Schlemms canal (1)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (1)     2.6.1 Production (1)     2.6.2 Outflow (3)       2.6.2.1 Trabecular meshwork (0)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (9)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (1)   2.9 Ciliary body (2)   2.10 Lens (1)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (3)   2.13 Retina and retinal nerve fibre layer (21)   2.14 Optic disc (17)   2.15 Optic nerve (3)   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 (1)   3.3 Immunohistochemistry (14)   3.4 Molecular genetics (4)     3.4.1 Linkage studies (15)     3.4.2 Gene studies (1)   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 (0)       9.4.11.2 Glaucomas in aphakia and pseudophakia (1)       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 (12)     9.4.20 Other (1) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (7) 11 Medical treatment (0)   11.1 General management, indication (10)   11.2 Cholinergic drugs (0)   11.3 Adrenergic drugs (0)     11.3.1 Epinephrine (0)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (8)     11.3.4 Betablocker (14)     11.3.5 Other (0)   11.4 Prostaglandins (23)   11.5 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Without tube implant (4)     12.8.2 With tube implant or other drainage devices (7)     12.8.3 Non-perforating (12)     12.8.4 Using laser (0)     12.8.5 Other (0)     12.8.10 Woundhealing antifibrosis (13)     12.8.11 Complications, endophthalmitis (8)   12.9 Trabeculotomy, goniotomy (0)   12.10 Cyclodestruction (5)   12.11 Cyclodialysis (3)   12.12 Cataract extraction (1)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (2)   12.14 Combined cataract extraction and glaucoma surgery (3)     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 (2)   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 (1)

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Abstract #10141 Published in IGR 6-1

Vasodilatory mechanism of unoprostone isopropyl on isolated rabbit ciliary artery

Yoshitomi T; Yamaji K; Ishikawa H; Ohnishi Y
Current Eye Research 2004; 28: 167-174

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PURPOSE: To clarify the vasodilatory mechanism of unoprostone isopropyl (unoprostone), a PG F2α related compound used for treatment of glaucoma, the authors investigated the effect of this drug and its metabolites on isolated rabbit ciliary artery in vitro. METHODS: Under the dissecting microscope, ciliary arteries were prepared from albino rabbit eyes and mounted in a myograph system. The effects of unoprostone isopropyl and other agents were investigated using isometric tension recording methods. RESULTS: Unoprostone induced a dose-dependent relaxation in ciliary arteries which were pre-contracted with high-K solution, 10 μm histamine or 10 microM PG F2α. Neither unoprostone metabolite M1 nor M2 had a relaxant effect on the precontracted vessels. Relaxation was unaffected by inhibition of adenylyl cyclase with SQ 22536, guanylyl cyclase with ODQ, or maxi-K channels with iberiotoxin. Pretreatment with unoprostone did not affect histamine-induced transient contractions in Ca²⁺ -free solution. However, SKF96365, a general Ca²⁺ channel blocker, evoked relaxation similar to unoprostone with respect to amplitude and rate of onset. CONCLUSIONS: Unoprostone, but not its metabolites M1 and M2, relaxed pre-contracted rabbit ciliary artery. The mechanism of vascular smooth muscle relaxation by unoprostone differs from that of IOP reduction and does not depend on adenylyl cyclase, guanylyl cyclase, or maxi-K channels. Relaxation may be mediated by inhibition of Ca²⁺ entry, possibly through capacitative Ca²⁺ channels.

Dr. T. Yoshitomi, Department of Ophthalmology, Wakayama Medical University, Wakayama, Japan. yoshitom@wakayama-med.ac.jp

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Classification:

11.4 Prostaglandins (Part of: 11 Medical treatment)

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