Dysfunctional regulation of ocular blood flow: A risk factor for glaucoma?

Danny Moore, Alon Harris, Darrell WuDunn, Nisha Kheradiya, Brent Siesky1Department of Ophthalmology, Indiana University School of Medicine, Indianapolis, IN, USAAbstract: Primary open angle glaucoma (OAG) is a multifactorial optic neuropathy characterized by progressive retinal ganglion cell death a...

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Autores principales: Danny Moore, Alon Harris, Darrell WuDunn, Nisha Kheradiya, Brent Siesky
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Lenguaje:EN
Publicado: Dove Medical Press 2008
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spelling oai:doaj.org-article:e4f2e1f70144440095a786b633e317df2021-12-02T02:48:04ZDysfunctional regulation of ocular blood flow: A risk factor for glaucoma?1177-54671177-5483https://doaj.org/article/e4f2e1f70144440095a786b633e317df2008-04-01T00:00:00Zhttp://www.dovepress.com/dysfunctional-regulation-of-ocular-blood-flow-a-risk-factor-for-glauco-a411https://doaj.org/toc/1177-5467https://doaj.org/toc/1177-5483Danny Moore, Alon Harris, Darrell WuDunn, Nisha Kheradiya, Brent Siesky1Department of Ophthalmology, Indiana University School of Medicine, Indianapolis, IN, USAAbstract: Primary open angle glaucoma (OAG) is a multifactorial optic neuropathy characterized by progressive retinal ganglion cell death and associated visual field loss. OAG is an emerging disease with increasing costs and negative outcomes, yet its fundamental pathophysiology remains largely undetermined. A major treatable risk factor for glaucoma is elevated intraocular pressure (IOP). Despite the medical lowering of IOP, however, some glaucoma patients continue to experience disease progression and subsequent irreversible vision loss. The scientific community continues to accrue evidence suggesting that alterations in ocular blood flow play a prominent role in OAG disease processes. This article develops the thesis that dysfunctional regulation of ocular blood flow may contribute to glaucomatous optic neuropathy. Evidence suggests that impaired vascular autoregulation renders the optic nerve head susceptible to decreases in ocular perfusion pressure, increases in IOP, and/or increased local metabolic demands. Ischemic damage, which likely contributes to further impairment in autoregulation, results in changes to the optic nerve head consistent with glaucoma. Included in this review are discussions of conditions thought to contribute to vascular regulatory dysfunction in OAG, including atherosclerosis, vasospasm, and endothelial dysfunction.Keywords: glaucoma, autoregulation, blood flow, atherosclerosis, vasospasm, endothelial dysfunction Danny MooreAlon HarrisDarrell WuDunnNisha KheradiyaBrent SieskyDove Medical PressarticleOphthalmologyRE1-994ENClinical Ophthalmology, Vol 2008, Iss Issue 4, Pp 849-861 (2008)
institution DOAJ
collection DOAJ
language EN
topic Ophthalmology
RE1-994
spellingShingle Ophthalmology
RE1-994
Danny Moore
Alon Harris
Darrell WuDunn
Nisha Kheradiya
Brent Siesky
Dysfunctional regulation of ocular blood flow: A risk factor for glaucoma?
description Danny Moore, Alon Harris, Darrell WuDunn, Nisha Kheradiya, Brent Siesky1Department of Ophthalmology, Indiana University School of Medicine, Indianapolis, IN, USAAbstract: Primary open angle glaucoma (OAG) is a multifactorial optic neuropathy characterized by progressive retinal ganglion cell death and associated visual field loss. OAG is an emerging disease with increasing costs and negative outcomes, yet its fundamental pathophysiology remains largely undetermined. A major treatable risk factor for glaucoma is elevated intraocular pressure (IOP). Despite the medical lowering of IOP, however, some glaucoma patients continue to experience disease progression and subsequent irreversible vision loss. The scientific community continues to accrue evidence suggesting that alterations in ocular blood flow play a prominent role in OAG disease processes. This article develops the thesis that dysfunctional regulation of ocular blood flow may contribute to glaucomatous optic neuropathy. Evidence suggests that impaired vascular autoregulation renders the optic nerve head susceptible to decreases in ocular perfusion pressure, increases in IOP, and/or increased local metabolic demands. Ischemic damage, which likely contributes to further impairment in autoregulation, results in changes to the optic nerve head consistent with glaucoma. Included in this review are discussions of conditions thought to contribute to vascular regulatory dysfunction in OAG, including atherosclerosis, vasospasm, and endothelial dysfunction.Keywords: glaucoma, autoregulation, blood flow, atherosclerosis, vasospasm, endothelial dysfunction
format article
author Danny Moore
Alon Harris
Darrell WuDunn
Nisha Kheradiya
Brent Siesky
author_facet Danny Moore
Alon Harris
Darrell WuDunn
Nisha Kheradiya
Brent Siesky
author_sort Danny Moore
title Dysfunctional regulation of ocular blood flow: A risk factor for glaucoma?
title_short Dysfunctional regulation of ocular blood flow: A risk factor for glaucoma?
title_full Dysfunctional regulation of ocular blood flow: A risk factor for glaucoma?
title_fullStr Dysfunctional regulation of ocular blood flow: A risk factor for glaucoma?
title_full_unstemmed Dysfunctional regulation of ocular blood flow: A risk factor for glaucoma?
title_sort dysfunctional regulation of ocular blood flow: a risk factor for glaucoma?
publisher Dove Medical Press
publishDate 2008
url https://doaj.org/article/e4f2e1f70144440095a786b633e317df
work_keys_str_mv AT dannymoore dysfunctionalregulationofocularbloodflowariskfactorforglaucoma
AT alonharris dysfunctionalregulationofocularbloodflowariskfactorforglaucoma
AT darrellwudunn dysfunctionalregulationofocularbloodflowariskfactorforglaucoma
AT nishakheradiya dysfunctionalregulationofocularbloodflowariskfactorforglaucoma
AT brentsiesky dysfunctionalregulationofocularbloodflowariskfactorforglaucoma
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