advertisement

---

1 General aspects (0)   1.1 Epidemiology (5)   1.2 Population genetics (1)   1.3 Pathogenesis (10)   1.4 Quality of life (6)   1.5 Glaucomas as cause of blindness (3)   1.6 Prevention and screening (4) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (1)   2.2 Cornea (9)   2.3 Sclera (1)   2.4 Anterior chamber angle (2)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (6)     2.5.2 Schlemms canal (2)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (3)       2.6.2.1 Trabecular meshwork (0)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (5)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (0)   2.9 Ciliary body (1)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (3)   2.13 Retina and retinal nerve fibre layer (6)   2.14 Optic disc (10)   2.15 Optic nerve (1)   2.16 Chiasma and retrochiasmal central nervous system (1)   2.17 Stem cells (0)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (3)   3.2 Electron microscopy (1)   3.3 Immunohistochemistry (10)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (13)     3.4.2 Gene studies (6)   3.5 Molecular biology incl. SiRNA (4)   3.6 Cellular biology (1)   3.7 Biochemistry (2)   3.8 Pharmacology (1)   3.9 Pathophysiology (5)   3.10 Immunobiology (0)   3.11 Pharmacogenetics (0)   3.12 Proteomics (0)   3.13 In vivo imaging (0)     3.13.1 Laser Scanning (0)       3.13.1.1 Confocal Scanning Laser Ophthalmoscopy (0)       3.13.1.2 Confocal Scanning Laser Polarimetry (0)     3.13.2 Optical Coherence Tomography (0)       3.13.2.1 Anterior Segment (0)       3.13.2.2 Posterior Segment (0)     3.13.3 RGC Imaging (0)     3.13.4 Other (0)   3.20 Other (1) 4 Tissue culture of ocular cells (0) 5 Experimental glaucoma; animal models (25)   5.1 Rodent (0)   5.2 Primates (0)   5.3 Other (0) 6 Clinical examination methods (0)   6.1 Intraocular pressure measurement; factors affecting IOP (22)     6.1.1 Devices, techniques (0)     6.1.2 Fluctuation, circadian rhythms (0)     6.1.3 Factors affecting IOP (0)   6.2 Tonography, aqueous flow measurement (see also 2.6) (1)   6.3 Biomicroscopy (slitlamp) (0)     6.3.1 Anterior segment (1)     6.3.2 Posterior segment (1)   6.4 Gonioscopy (3)   6.5 Ophthalmoscopy (0)   6.6 Visual field examination and other visual function tests (0)     6.6.1 Conventional manual (0)     6.6.2 Automated (5)     6.6.3 Special methods (e.g. color, contrast, SWAP etc.) (23)   6.7 Electro-ophthalmodiagnosis (6)   6.8 Photography (0)     6.8.1 Anterior segment (0)     6.8.2 Posterior segment (3)   6.9 Computerized image analysis (0)     6.9.1 Laser scanning (20)       6.9.1.1 Confocal Scanning Laser Ophthalmoscopy (0)       6.9.1.2 Confocal Scanning Laser Polarimetry (0)     6.9.2 Optical coherence tomography (15)       6.9.2.1 Anterior (0)       6.9.2.2 Posterior (0)     6.9.5 Other (0)   6.10 Fluorescein (ICG) angiography (0)     6.10.1 Anterior segment (0)     6.10.2 Posterior segment (0)   6.11 Bloodflow measurements (14)   6.12 Ultrasonography and ultrasound biomicroscopy (1)   6.13 Provocative tests (1)   6.19 Telemedicine (0)   6.20 Progression (9)   6.30 Other (0) 8 Refractive errors in relation to glaucoma (1)   8.1 Myopia (3)   8.2 Hypermetropia (0)   8.3 Contact lenses (1)   8.4 Refractive surgical procedures (3)   8.5 Other (0) 9 Clinical forms of glaucomas (0)   9.1 Developmental glaucomas (2)     9.1.1 Congenital glaucoma, Buphthalmos (4)     9.1.2 Juvenile glaucoma (1)     9.1.3 Syndromes of Axenfeld, Rieger, Peters, aniridia (4)     9.1.4 Other (0)   9.2 Primary open angle glaucomas (0)     9.2.1 Ocular hypertension (2)     9.2.2 Other risk factors for glaucoma (14)     9.2.3 Open angle glaucoma with elevated IOP (1)     9.2.4 Normal pressure glaucoma (6)   9.3 Primary angle closure glaucomas (10)     9.3.1 Acute primary angle closure glaucoma (pupillary block) (2)     9.3.2 Chronic primary angle closure glaucoma (pupillary block) (2)     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 (1)   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) (3)       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 (0)       9.4.3.1 Pigmentary glaucoma (2)       9.4.3.5 Other (0)     9.4.4 Glaucomas associated with disorders of the lens (1)       9.4.4.1 Exfoliation syndrome (4)       9.4.4.2 Glaucomas associated with cataracts (1)       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 (0)       9.4.5.5 Other (0)     9.4.6 Glaucomas associated with inflammation, uveitis (2)     9.4.7 Glaucomas associated with ocular trauma (1)     9.4.8 Glaucomas associated 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 (0)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (1)     9.4.15 Glaucoma in relation to systemic disease (6)     9.4.20 Other (0) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (6) 11 Medical treatment (0)   11.1 General management, indication (12)   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 (7)     11.3.4 Betablocker (7)     11.3.5 Other (0)   11.4 Prostaglandins (20)   11.5 Carbonic anhydrase inhibitors (1)     11.5.1 Systemic (0)     11.5.2 Topical (8)   11.6 Osmotic treatment (0)   11.7 Treatment of bloodflow (3)   11.8 Neuroprotection (7)   11.9 Gene therapy (0)   11.13 Combination therapy (0)     11.13.1 Betablocker and pilocarpine (0)     11.13.2 Betablocker and carbon anhydrase inhibitor (0)     11.13.3 Betablocker and brimonidine (0)     11.13.4 Betablocker and prostaglandin (0)     11.13.5 Other (0)   11.14 Investigational drugs; pharmacological experiments (7)   11.15 Other drugs in relation to glaucoma (2)   11.16 Vehicles, delivery systems, pharmacokinetics, formulation (3)   11.17 Cooperation with medical therapy e.g. persistency, compliance, adherence (3)   11.20 Other (2) 12 Surgical treatment (0)   12.1 General management, indication (5)   12.2 Laser iridotomy (3)   12.3 Laser iridoplasty (1)   12.4 Laser trabeculoplasty and other laser treatment of the angle (2)   12.7 Surgical iridectomy (0)   12.8 Filtering surgery (2)     12.8.1 Without tube implant (8)     12.8.2 With tube implant or other drainage devices (11)     12.8.3 Non-perforating (5)     12.8.4 Using laser (0)     12.8.5 Other (0)     12.8.10 Woundhealing antifibrosis (16)     12.8.11 Complications, endophthalmitis (8)   12.9 Trabeculotomy, goniotomy (1)   12.10 Cyclodestruction (4)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (3)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (0)     12.14.3 Phacoemulsification (10)   12.15 Capsulotomy (0)   12.16 Vitrectomy (0)   12.17 Anesthesia (1)   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 (6)

---

Abstract #11722 Published in IGR 7-1

Enhanced endothelium derived hyperpolarising factor activity in resistance arteries from normal pressure glaucoma patients: implications for vascular function in the eye

Cleary C; Buckley CH; Henry E; McLoughlin P; O'Brien C; Hadoke PW
British Journal of Ophthalmology 2005; 89: 223-228

See also comment(s) by Alon Harris •

---

BACKGROUND/AIMS: Endothelial cell dysfunction in the ocular circulation may contribute to normal pressure glaucoma (NPG). This study aimed to investigate the contributions made by endothelium derived relaxing factors to relaxation of (1) subcutaneous resistance arteries from patients with NPG, and (2) porcine ciliary arteries. METHODS: Human gluteal resistance arteries were isolated from seven patients with NPG and matched controls. Human and porcine arteries produced endothelium dependent relaxation when exposed to acetylcholine (ACh) (10^-9 -3 x 10^-5 M) or bradykinin (10^-10 -3 x 10^-6 M). Pharmacological agents were used to inhibit the nitric oxide pathway (l-arginine analogues, soluble guanylate cyclase inhibitor), endothelium derived hyperpolarising factor (EDHF) activity (potassium channel antagonists), and prostaglandin synthesis (cyclo-oxygenase inhibitors). RESULTS: In all arteries, endothelium dependent relaxation was attenuated by nitric oxide (NO) inhibition or potassium channel blockade, but not by cyclo-oxygenase inhibition. Inhibition of ACh mediated relaxation by potassium channel antagonists was greater (p < 0.05) in patients with NPG (Emax, 55.4% (SD 8.16%) relaxation, n = 4) than controls (Emax, 81.8% (6.0%), n = 5). In contrast, combined inhibition of NO synthase (NOS) and cyclo-oxygenase produced similar inhibition of ACh mediated relaxation in both groups. CONCLUSIONS: The enhanced contribution of EDHF to ACh mediated relaxation in systemic resistance arteries from NPG patients may contribute to the maintained endothelium mediated relaxation in these vessels. EDHF also contributes significantly to bradykinin mediated relaxation in porcine ocular ciliary arteries. Therefore, similar changes in the balance of relaxing factors in the ocular circulation could influence the response of the eye to vascular endothelial dysfunction in NPG.

Dr. C. Cleary, Department of Ophthalmology, Conway Institute, University College Dublin, Ireland

---

Classification:

6.11 Bloodflow measurements (Part of: 6 Clinical examination methods)
9.2.2 Other risk factors for glaucoma (Part of: 9 Clinical forms of glaucomas > 9.2 Primary open angle glaucomas)
9.2.4 Normal pressure glaucoma (Part of: 9 Clinical forms of glaucomas > 9.2 Primary open angle glaucomas)

---

• ← Previous
• Next →

---