The impact of ocular blood flow in glaucoma

Flammer, Josef; Orgül, Selim; Costa, Vital Paulino; Orzalesi, N.; Krieglstein, Günter K.; Serra, Lídia; Renard, Jean‐Paul; Stefánsson, Einar

doi:10.1016/s1350-9462(02)00008-3

Cited by 1,513 publications

(1,307 citation statements)

References 327 publications

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“…Identification of individuals with FS may be clinically relevant as systemic vascular dysregulation has been associated with several ocular diseases [102], including glaucoma [103][104][105][106][107][108][109][110], central serous chorioretinopathy [111], and central retinal vein occlusion. The role of the endothelium as major pathomechanistic red line connects many dots that outline a sketch of FS.…”

Section: Endothelial Dysregulation In Flammer Syndromementioning

confidence: 99%

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

et al. 2017

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The endothelium has increasingly been recognized as a smart barrier and a key regulator of blood flow in microand macrovascular beds. Endothelial dysfunction marks a stage of atherosclerosis and is an important prognostic marker for cardiovascular disease. Yet, some people who tend to be slim and physically active and with rather low blood pressure show a propensity to respond to certain stimuli such as emotional stress with endothelial-mediated vascular dysregulation (Flammer syndrome). This leads to characteristic vascular symptoms such as cold hands but also a risk for vascularmediated diseases such as normal-tension glaucoma. It is the aim of this review to delineate the differences between Flammer syndrome and its Bcounterpart^endothelial dysfunction in the context of cardiovascular diseases.

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Section: Endothelial Dysregulation In Flammer Syndromementioning

confidence: 99%

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

et al. 2017

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“…119 It should be noted, however, that glaucoma can develop in patients with normal intraocular pressure. 119,120 In patients with age-related macular degeneration, reductions in choroidal blood flow, but not retinal flow, have been observed. [121][122][123][124] These reports support the hypothesis that a primary cause of age-related macular degeneration may be a diminished supply of oxygen and nutrients and a decrease in the clearance of waste products from the pigment epithelium and the outer retina caused by reduced choroidal blood flow, possibly arising from stiffening of the sclera and Bruch's membrane due to lipid deposition.…”

Section: Modulation Of Functional Hyperemia In the Retina Oxygen Modumentioning

confidence: 99%

Functional Hyperemia and Mechanisms of Neurovascular Coupling in the Retinal Vasculature

Newman

2013

J Cereb Blood Flow Metab

196

162

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The retinal vasculature supplies cells of the inner and middle layers of the retina with oxygen and nutrients. Photic stimulation dilates retinal arterioles producing blood flow increases, a response termed functional hyperemia. Despite recent advances, the neurovascular coupling mechanisms mediating the functional hyperemia response in the retina remain unclear. In this review, the retinal functional hyperemia response is described, and the cellular mechanisms that may mediate the response are assessed. These neurovascular coupling mechanisms include neuronal stimulation of glial cells, leading to the release of vasoactive arachidonic acid metabolites onto blood vessels, release of potassium from glial cells onto vessels, and production and release of nitric oxide (NO), lactate, and adenosine from neurons and glia. The modulation of neurovascular coupling by oxygen and NO are described, and changes in functional hyperemia that occur with aging and in diabetic retinopathy, glaucoma, and other pathologies, are reviewed. Finally, outstanding questions concerning retinal blood flow in health and disease are discussed. In lower vertebrates that have thinner retinas, including amphibians, reptiles, and some mammals, the retinal vasculature is absent and the choroidal circulation supplies the entire retina. 2 The choroidal circulation is supplied by the long and short ciliary arteries and the anterior ciliary arteries, which feed the large arteries in the outer portion of the choroid. 3 These arteries branch into smaller vessels, which, in turn, feed the highly anastomosed choriocapillaris network lying at the inner border of the choroid, adjacent to the retinal pigment epithelium and retinal photoreceptors. The total blood flow supplying the choroid is much greater than that supplying the retina (606 vs. 25 mg/min/ whole tissue 4 ), to meet the high metabolic demands of the photoreceptors. 5 The retinal vasculature is supplied by the central retinal artery, which enters the retina with the optic nerve at the optic disc. The artery branches into radial arterioles and smaller vessels on the vitreal surface of the retina. 3 Pre-capillary arterioles and capillaries ramify from these surface vessels and form anastomotic networks in the ganglion cell layer, just beneath the retinal surface, and deeper in the inner nuclear layer, supplying horizontal cells, bipolar cells, amacrine cells, and Mü ller glial cells. Blood is returned through radial venules on the retinal surface that empty into the central retinal vein in the optic nerve. Journal of Cerebral BloodThe retinal and choroidal vasculatures differ in several respects. Retinal vessels lack autonomic innervation, 6,7 whereas the choroidal circulation is innervated by both sympathetic and parasympathetic

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“…5 Consequently, previous studies focused on vascular, immunologic, and neurotoxic factors, which have subsequently been shown to contribute to the pathogenesis of POAG. [6][7][8] In recent years, tumour necrosis factor-a (TNF-a), a major immunomodulator and proinflammatory cytokine, has been suggested to participate in the apoptotic death of retinal ganglion cells in glaucoma patients. Tezel et al 10 and Tezel and Wax 11 reported an upregulation of TNF-a and TNF-a receptor-1 in optic nerve heads and retina sections of glaucomatous eyes.…”

Section: Introductionmentioning

confidence: 99%

TNF-α promoter polymorphisms and primary open-angle glaucoma

Mossböck

Weger

Moray

et al. 2005

Eye

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Purpose Primary open-angle glaucoma (POAG) is a multifactorial optic neuropathy with a strong hereditary component. Recent studies suggested a role for tumour necrosis factor-a (TNF-a) in the pathogenesis of POAG. The purpose of the present study was to investigate a hypothesized association between the TNF-a À308G4A and À238G4A gene polymorphisms and the presence of POAG in a Caucasian population. Methods The present case-control study comprised 114 unrelated patients with POAG and 228 healthy control subjects, matched for age and gender. Genotyping of the TNF-a À308G4A and À238G4A polymorphisms was performed using polymerase chain reaction. Results Allelic frequencies and genotype distributions of both the TNF-a À308G4A and À238G4A gene polymorphisms did not significantly differ between patients with POAG and control subjects. Presence of the TNF-a À308A-allele was associated with an odds ratio (OR) of 0.96 for POAG, whereas an OR of 0.52 was found among carriers of the TNF-a À238A-allele. Conclusion Our data suggest that none of the investigated TNF-a gene polymorphisms is a major risk factor among Caucasian patients with POAG.

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The impact of ocular blood flow in glaucoma

Cited by 1,513 publications

References 327 publications

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

Functional Hyperemia and Mechanisms of Neurovascular Coupling in the Retinal Vasculature

TNF-α promoter polymorphisms and primary open-angle glaucoma

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