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Article: Total retinal nitric oxide production is increased in intraocular pressure-elevated rats

TitleTotal retinal nitric oxide production is increased in intraocular pressure-elevated rats
Authors
Issue Date2002
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexer
Citation
Experimental Eye Research, 2002, v. 75 n. 4, p. 401-406 How to Cite?
AbstractNitric oxide (NO) is a well-known vaso-dilator but its regulation in the retina is unclear. This study was conducted to quantify total NO production and retinal ganglion cell (RGC) loss in an experimental glaucoma model. Three quarters of the peri-limbal/episcleral drainage vessels and anterior angle (right eyes) of Sprague-Dawley rats were thermally blocked using laser irradiation, while the left eyes served as controls. We measured the intraocular pressure (IOP) of both eyes using a digital tonometer (Tonopen) 21, 28 and 35 days after the laser treatment. After 35 days, we determined the total NO level in retinas and remaining ocular tissues for the laser-treated and control eyes using a spectro-photometric assay. The viable RGC numbers were also determined by counting the cell bodies stained retrogradely by fluoro-gold. The laser treatment significantly increased the lOP 2.0-2.6× throughout the whole period of measurements (P < 0.0001). The mean total RGC number decreased significantly from 98 725 ± 5383 (±S.E. (M.)) to 69 276 ± 5592, or 29.8% reduction, in the laser-treated eyes after 35 days (P = 0.008). The mean total NO level in the laser-treated retina was significantly increased by 2.4× compared with controls (P = 0.016), but no significant difference was found in the eyecups (P > 0.05). Laser treatment resulted in significant IOP elevation and RGC loss, suggesting that thermal coagulation of the perilimbal region may provide an alternate protocol for glaucoma study. NO level was increased by two-fold in the retina but not in other ocular tissues. Since NO is capable of producing powerful peroxynitrite anions and hydroxyl radicals, elevated level of NO has a potential role in glaucoma. © 2002 Elsevier Science Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/67457
ISSN
2015 Impact Factor: 2.998
2015 SCImago Journal Rankings: 1.218
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSiu, AWen_HK
dc.contributor.authorLeung, MCPen_HK
dc.contributor.authorHo To, Cen_HK
dc.contributor.authorSiu, FKWen_HK
dc.contributor.authorJi, JZen_HK
dc.contributor.authorFai So, Ken_HK
dc.date.accessioned2010-09-06T05:55:18Z-
dc.date.available2010-09-06T05:55:18Z-
dc.date.issued2002en_HK
dc.identifier.citationExperimental Eye Research, 2002, v. 75 n. 4, p. 401-406en_HK
dc.identifier.issn0014-4835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67457-
dc.description.abstractNitric oxide (NO) is a well-known vaso-dilator but its regulation in the retina is unclear. This study was conducted to quantify total NO production and retinal ganglion cell (RGC) loss in an experimental glaucoma model. Three quarters of the peri-limbal/episcleral drainage vessels and anterior angle (right eyes) of Sprague-Dawley rats were thermally blocked using laser irradiation, while the left eyes served as controls. We measured the intraocular pressure (IOP) of both eyes using a digital tonometer (Tonopen) 21, 28 and 35 days after the laser treatment. After 35 days, we determined the total NO level in retinas and remaining ocular tissues for the laser-treated and control eyes using a spectro-photometric assay. The viable RGC numbers were also determined by counting the cell bodies stained retrogradely by fluoro-gold. The laser treatment significantly increased the lOP 2.0-2.6× throughout the whole period of measurements (P < 0.0001). The mean total RGC number decreased significantly from 98 725 ± 5383 (±S.E. (M.)) to 69 276 ± 5592, or 29.8% reduction, in the laser-treated eyes after 35 days (P = 0.008). The mean total NO level in the laser-treated retina was significantly increased by 2.4× compared with controls (P = 0.016), but no significant difference was found in the eyecups (P > 0.05). Laser treatment resulted in significant IOP elevation and RGC loss, suggesting that thermal coagulation of the perilimbal region may provide an alternate protocol for glaucoma study. NO level was increased by two-fold in the retina but not in other ocular tissues. Since NO is capable of producing powerful peroxynitrite anions and hydroxyl radicals, elevated level of NO has a potential role in glaucoma. © 2002 Elsevier Science Ltd.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexeren_HK
dc.relation.ispartofExperimental Eye Researchen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Counten_HK
dc.subject.meshGlaucoma - metabolism - physiopathologyen_HK
dc.subject.meshIntraocular Pressure - physiologyen_HK
dc.subject.meshNitric Oxide - biosynthesisen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshRetina - metabolismen_HK
dc.subject.meshRetinal Ganglion Cells - metabolismen_HK
dc.titleTotal retinal nitric oxide production is increased in intraocular pressure-elevated ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-4835&volume=75&spage=401&epage=406&date=2002&atitle=Total+retinal+nitric+oxide+production+is+increased+in+intraocular+pressure-elevated+ratsen_HK
dc.identifier.emailFai So, K:hrmaskf@hkucc.hku.hken_HK
dc.identifier.authorityFai So, K=rp00329en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0014-4835(02)92029-4en_HK
dc.identifier.pmid12387787-
dc.identifier.scopuseid_2-s2.0-0036034481en_HK
dc.identifier.hkuros74639en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036034481&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume75en_HK
dc.identifier.issue4en_HK
dc.identifier.spage401en_HK
dc.identifier.epage406en_HK
dc.identifier.isiWOS:000179086900003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridSiu, AW=7006727808en_HK
dc.identifier.scopusauthoridLeung, MCP=7201943351en_HK
dc.identifier.scopusauthoridHo To, C=15825248400en_HK
dc.identifier.scopusauthoridSiu, FKW=6701518486en_HK
dc.identifier.scopusauthoridJi, JZ=7201362425en_HK
dc.identifier.scopusauthoridFai So, K=34668391300en_HK

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