Response of Retinal Vessel Diameters to Flicker Stimulation in Patients with Early Open Angle Glaucoma

Garhöfer, Gerhard; Zawinka, Claudia; Resch, Hemma; Huemer, Karl-Heinz; Schmetterer, Leopold; Dorner, Guido T.

doi:10.1097/00061198-200408000-00013

Cited by 104 publications

(104 citation statements)

References 16 publications

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“…117 Also, in the early stages of the disease, a reduction in flicker-evoked dilation of retinal venules but not arterioles is observed in patients. 118 These observations support the hypothesis that the pathologic changes associated with glaucoma may be due, at least in some instances, to retinal ischemia caused by the increase in intraocular pressure and the resulting decrease in perfusion pressure, leading to a decrease in retinal blood flow. 119 It should be noted, however, that glaucoma can develop in patients with normal intraocular pressure.…”

Section: Modulation Of Functional Hyperemia In the Retina Oxygen Modusupporting

confidence: 81%

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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Section: Modulation Of Functional Hyperemia In the Retina Oxygen Modusupporting

confidence: 81%

Functional Hyperemia and Mechanisms of Neurovascular Coupling in the Retinal Vasculature

Newman

2013

J Cereb Blood Flow Metab

196

162

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“…192 Indeed, neurovascular coupling in the retina appears to be disturbed early in glaucoma. 190,193,194 In principle, restoration of neurovascular coupling may be an attractive approach for glaucoma, but the mechanisms that lead to its breakdown are poorly understood.…”

Section: Other Approachesmentioning

confidence: 99%

Pharmacotherapy of Glaucoma

Schmidl

Schmetterer²,

Garhöfer³

et al. 2015

Journal of Ocular Pharmacology and Therapeutics

136

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Glaucoma is a group of diseases involving the optic nerve and associated structures, which is characterized by progressive visual field loss and typical changes of the optic nerve head (ONH). The only known treatment of the disease is reduction of intraocular pressure (IOP), which has been shown to reduce glaucoma progression in a variety of large-scale clinical trials. Nowadays, a relatively wide array of topical antiglaucoma drugs is available, including prostaglandin analogues, carbonic anhydrase inhibitors, beta-receptor antagonists, adrenergic agonists, and parasympathomimetics. In clinical routine, this allows for individualized treatment taking risk factors, efficacy, and safety into account. A major challenge is related to adherence to therapy. Sustained release devices may help minimize this problem but are not yet available for clinical routine use. Another hope arises from non-IOP-related treatment concepts. In recent years, much knowledge has been gained regarding the molecular mechanisms that underlie the disease process in glaucoma. This also strengthens the hope that glaucoma therapy beyond IOP lowering will become available. Implementing this concept with clinical trials remains, however, a challenge.

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“…Previous clinical studies using the DVA have shown the impaired dilation to this flicker, reflecting possibly endothelial dysfunction, is associated with systemic diseases, 13 including hypertension 8 and diabetes, 14 and ocular diseases, such as diabetic retinopathy 14 and glaucoma. 15 However, although DVA has previously been shown to be reproducible in whites, 16 there have been no similar data in groups/races other than whites, including Asians. In this study, we aim to assess the reproducibility of the retinal vessel dilation in response to flicker-light, as measured by the DVA in Asians and compare the corresponding reproducibility reported in whites.…”

Section: Introductionmentioning

confidence: 97%

Reproducibility of the Retinal Vascular Response to Flicker Light in Asians

Nguyên¹,

Kreis²,

Kawasaki³

et al. 2009

Current Eye Research

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Response of Retinal Vessel Diameters to Flicker Stimulation in Patients with Early Open Angle Glaucoma

Abstract: Flicker-induced vasodilatation of retinal veins is significantly diminished in patients with glaucoma compared with healthy volunteers. This indicates that regulation of retinal vascular tone is impaired in patients with early glaucoma, independently of antiglaucoma medication.

Cited by 104 publications

References 16 publications

Functional Hyperemia and Mechanisms of Neurovascular Coupling in the Retinal Vasculature

Functional Hyperemia and Mechanisms of Neurovascular Coupling in the Retinal Vasculature

Pharmacotherapy of Glaucoma

Reproducibility of the Retinal Vascular Response to Flicker Light in Asians

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