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1 General aspects (1)   1.1 Epidemiology (14)   1.2 Population genetics (2)   1.3 Pathogenesis (1)   1.4 Quality of life (20)   1.5 Glaucomas as cause of blindness (8)   1.6 Prevention and screening (13) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (10)   2.2 Cornea (23)   2.3 Sclera (16)   2.4 Anterior chamber angle (7)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (15)     2.5.2 Schlemms canal (1)     2.5.3 Scleral outlet channels (1)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (1)       2.6.2.1 Trabecular meshwork (4)       2.6.2.2 Uveoscleral (1)     2.6.3 Compostion (6)   2.7 Episcleral veins and venous pressure (2)   2.8 Iris (6)   2.9 Ciliary body (0)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (18)   2.13 Retina and retinal nerve fibre layer (37)   2.14 Optic disc (42)   2.15 Optic nerve (2)   2.16 Chiasma and retrochiasmal central nervous system (13)   2.17 Stem cells (5)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (0)   3.2 Electron microscopy (2)   3.3 Immunohistochemistry (2)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (0)     3.4.2 Gene studies (30)   3.5 Molecular biology incl. SiRNA (19)   3.6 Cellular biology (36)   3.7 Biochemistry (10)   3.8 Pharmacology (21)   3.9 Pathophysiology (14)   3.10 Immunobiology (6)   3.11 Pharmacogenetics (0)   3.12 Proteomics (3)   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 (1)     3.13.4 Other (2)   3.20 Other (0) 4 Tissue culture of ocular cells (0) 5 Experimental glaucoma; animal models (0)   5.1 Rodent (33)   5.2 Primates (6)   5.3 Other (7) 6 Clinical examination methods (0)   6.1 Intraocular pressure measurement; factors affecting IOP (0)     6.1.1 Devices, techniques (19)     6.1.2 Fluctuation, circadian rhythms (10)     6.1.3 Factors affecting IOP (22)   6.2 Tonography, aqueous flow measurement (see also 2.6) (1)   6.3 Biomicroscopy (slitlamp) (0)     6.3.1 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surgery (0)     12.8.1 Without tube implant (17)     12.8.2 With tube implant or other drainage devices (68)     12.8.3 Non-perforating (13)     12.8.4 Using laser (0)     12.8.5 Other (1)     12.8.10 Woundhealing antifibrosis (17)     12.8.11 Complications, endophthalmitis (15)   12.9 Trabeculotomy, goniotomy (25)   12.10 Cyclodestruction (11)   12.11 Cyclodialysis (1)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (14)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (0)     12.14.3 Phacoemulsification (19)   12.15 Capsulotomy (0)   12.16 Vitrectomy (2)   12.17 Anesthesia (2)   12.20 Other (2) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (2)   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 (8) 15 Miscellaneous (37)

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Abstract #82687 Published in IGR 20-4

Impact of nitric oxide's bidirectional role on glaucoma: focus on Helicobacter pylori-related nitrosative stress

Papaefthymiou A; Doulberis M; Katsinelos P; Liatsos C; Polyzos SA; Kotronis G; Papanikolaou K; Kountouras J
Annals of the New York Academy of Science 2019; 0:

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Nitric oxide (NO), a small molecule generated ubiquitously, targets a plethora of tissues to regulate both physiological and pathophysiological functions. NO overproduction, stimulated by microenvironmental conditions, is the main component that dysregulates the tight balance between its beneficial and damaging roles in ocular homeostasis. Considering the protective functions of NO against glaucoma, its endogenous release facilitates aqueous humor drainage and regulates ocular blood flow, maintaining a normal intraocular pressure. NO overproduction generates free radicals, such as peroxynitrite, which induce a vicious circle of vascular disharmony and dysregulation, transient ischemia, nitrosative stress, neuronal degeneration, and permanent glaucomatic injury. Helicobacter pylori (Hp) is considered a burdening factor of glaucoma. NO overproduction and possible systematic dispersion in Hp infection (Hp-I) could suggest a potential pathophysiological bridge between these conditions. In this review, we aim to elucidate the role of NO in glaucoma with respect to Hp-I, with the aim to stimulate further studies.

Department of Gastroenterology, 401 General Military Hospital of Athens, Athens, Greece.

Full article

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Classification:

3.9 Pathophysiology (Part of: 3 Laboratory methods)
3.8 Pharmacology (Part of: 3 Laboratory methods)

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