The impact of ocular blood flow in glaucoma

The impact of ocular blood flow in glaucoma Two principal theories for the pathogenesis of glaucomatous optic neuropathy (GON) have been described—a mechanical and a vascular theory. Both have been defended by various research groups over the past 150 years. According to the mechanical theory, increased intraocular pressure (IOP) causes stretching of the laminar beams and damage to retinal ganglion cell axons. The vascular theory of glaucoma considers GON as a consequence of insufficient blood supply due to either increased IOP or other risk factors reducing ocular blood flow (OBF). A number of conditions such as congenital glaucoma, angle-closure glaucoma or secondary glaucomas clearly show that increased IOP is sufficient to lead to GON. However, a number of observations such as the existence of normal-tension glaucoma cannot be satisfactorily explained by a pressure theory alone. Indeed, the vast majority of published studies dealing with blood flow report a reduced ocular perfusion in glaucoma patients compared with normal subjects. The fact that the reduction of OBF often precedes the damage and blood flow can also be reduced in other parts of the body of glaucoma patients, indicate that the hemodynamic alterations may at least partially be primary. The major cause of this reduction is not atherosclerosis, but rather a vascular dysregulation, leading to both low perfusion pressure and insufficient autoregulation. This in turn may lead to unstable ocular perfusion and thereby to ischemia and reperfusion damage. This review discusses the potential role of OBF in glaucoma and how a disturbance of OBF could increase the optic nerve's sensitivity to IOP. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Progress in Retinal and Eye Research Elsevier

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Publisher
Elsevier
Copyright
Copyright © 2002 Elsevier Science Ltd
ISSN
1350-9462
eISSN
1873-1635
D.O.I.
10.1016/S1350-9462(02)00008-3
Publisher site
See Article on Publisher Site

Abstract

Two principal theories for the pathogenesis of glaucomatous optic neuropathy (GON) have been described—a mechanical and a vascular theory. Both have been defended by various research groups over the past 150 years. According to the mechanical theory, increased intraocular pressure (IOP) causes stretching of the laminar beams and damage to retinal ganglion cell axons. The vascular theory of glaucoma considers GON as a consequence of insufficient blood supply due to either increased IOP or other risk factors reducing ocular blood flow (OBF). A number of conditions such as congenital glaucoma, angle-closure glaucoma or secondary glaucomas clearly show that increased IOP is sufficient to lead to GON. However, a number of observations such as the existence of normal-tension glaucoma cannot be satisfactorily explained by a pressure theory alone. Indeed, the vast majority of published studies dealing with blood flow report a reduced ocular perfusion in glaucoma patients compared with normal subjects. The fact that the reduction of OBF often precedes the damage and blood flow can also be reduced in other parts of the body of glaucoma patients, indicate that the hemodynamic alterations may at least partially be primary. The major cause of this reduction is not atherosclerosis, but rather a vascular dysregulation, leading to both low perfusion pressure and insufficient autoregulation. This in turn may lead to unstable ocular perfusion and thereby to ischemia and reperfusion damage. This review discusses the potential role of OBF in glaucoma and how a disturbance of OBF could increase the optic nerve's sensitivity to IOP.

Journal

Progress in Retinal and Eye ResearchElsevier

Published: Jul 1, 2002

References

  • Expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases in human optic nerve head astrocytes
    Agapova, O.A.; Ricard, C.S.; Salvador-Silva, M.; Hernandez, M.R.
  • Scanning laser ophthalmoscopy-based evaluation of epipapillary velocities
    Arend, O.; Harris, A.; Martin, B.J.; Remky, A.
  • Erythrocyte deformability in high-tension and normal tension glaucoma
    Ates, H.; Uretmen, O.; Temiz, A.; Andac, K.
  • Ambulatory blood pressure monitoring in glaucoma patients. The nocturnal systolic dip and its relationship with disease progression
    Collignon, N.; Dewe, W.; Guillaume, S.; Collignon-Brach, J.
  • Risk factors for progression of visual field abnormalities in normal-tension glaucoma
    Drance, S.; Anderson, D.R.; Schulzer, M.
  • Autoregulation in the human retinal circulation
    Dumskyj, M.J.; Eriksen, J.E.; Dore, C.J.; Kohner, E.M.
  • Assessment of optic disk blood flow in patients with open-angle glaucoma
    Findl, O.; Rainer, G.; Dallinger, S.; Dorner, G.; Polak, K.; Kiss, B.; Georgopoulos, M.; Vass, C.; Schmetterer, L.
  • Glaucomatous optic neuropathy
    Flammer, J.
  • Optic nerve blood-flow abnormalities in glaucoma
    Flammer, J.; Orgül, S.
  • Vascular dysregulation
    Flammer, J.; Haefliger, I.O.; Orgül, S.; Resink, T.
  • Vasospasm, its role in the pathogenesis of diseases with particular reference to the eye
    Flammer, J.; Pache, M.; Resink, T.
  • Macular hemodynamic responses to short-term acute exercise in young healthy adults
    Forcier, P.; Kergoat, H.; Lovasik, J.V.
  • Ocular haemodynamics in glaucoma associated with high myopia
    Galassi, F.; Sodi, A.; Ucci, F.; Harris, A.; Chung, H.S.
  • Retrobulbar blood flow in glaucoma patients with nocturnal over-dipping in systemic blood pressure
    Gherghel, D.; Orgül, S.; Gugleta, K.; Flammer, J.
  • Nocturnal hypotension
    Graham, S.L.; Drance, S.M.
  • Modulation of Heidelberg retinal flowmeter parameter flow at the papilla of healthy subjects
    Haefliger, I.O.; Lietz, A.; Griesser, S.M.; Ulrich, A.; Schotzau, A.; Hendrickson, P.; Flammer, J.
  • Endothelium-dependent vasoactive modulation in the ophthalmic circulation
    Haefliger, I.O.; Flammer, J.; Bény, J.-L.; Lüscher, T.
  • Progress in measurement of ocular blood flow and relevance to our understanding of glaucoma and age-related macular degeneration
    Harris, A.; Chung, H.S.; Ciulla, T.A.; Kagemann, L.
  • Blood supply of the optic nerve head
    Hayreh, S.S.
  • Retinal and optic nerve head ischemic disorders and atherosclerosis
    Hayreh, S.S.
  • The optic nerve head in glaucoma
    Hernandez, M.R.
  • Risk factors for open-angle glaucoma
    Kaimbo, D.K.; Buntinx, F.; Missotten, L.
  • Systemic hypotension
    Kaiser, H.J.; Flammer, J.
  • Systemic blood pressure in glaucoma patients
    Kaiser, H.J.; Flammer, J.; Graf, T.; Stümpfig, D.
  • Vasospasm
    Kaiser, H.J.; Flammer, J.; Messerli, J.
  • Using the POBF as an index of interocular blood flow effects during unilateral vascular stress
    Kergoat, H.
  • A comparison of ocular blood flow in untreated primary open-angle glaucoma and ocular hypertension
    Kerr, J.; Nelson, P.; O’Brien, C.
  • Functional role of nitric oxide in regulation of ocular blood flow
    Koss, M.C.
  • Expression of nitric oxide synthase-2 (NOS-2) in reactive astrocytes of the human glaucomatous optic nerve head
    Liu, B.; Neufeld, A.H.
  • Portable ocular laser Doppler red blood cell velocimeter
    Logean, E.; Geiser, M.H.; Petrig, B.L.; Riva, C.E.
  • Alterations of autonomic nervous activity preceding nocturnal variant angina
    Miwa, K.; Igawa, A.; Miyagi, Y.; Nakagawa, K.; Inoue, H.
  • Experimental optic cup enlargement caused by endothelin-1 induced chronic optic nerve head ischemia
    Oku, H.; Sugiyama, T.; Kojima, S.; Watanabe, T.; Azuma, I.
  • Physiology of perfusion as it relates to the optic nerve head
    Orgül, S.; Gugleta, K.; Flammer, J.
  • Effect of timolol, latanoprost and dorzolamide on circadian IOP in glaucoma or ocular hypertension (1)
    Orzalesi, N.; Rossetti, L.; Invernizzi, T.; Bottoli, A.; Autelitano, A.
  • Increased endothelin-1 plasma levels in giant cell arteritis
    Pache, M.; Kaiser, H.J.; Haufschild, T.; Lübeck, P.; Flammer, J.
  • Laser Doppler flowmetry in the optic nerve head
    Petrig, B.L.; Riva, C.E.
  • Optic nerve blood flow is diminished in eyes of primary open-angle glaucoma suspects
    Piltz-Seymour, J.R.; Grunwald, J.E.; Hariprasad, S.M.; Dupont, J.
  • Interocular difference in progression of glaucoma correlates with interocular differences in retrobulbar circulation
    Schumann, J.; Orgül, S.; Gugleta, K.; Dubler, B.; Flammer, J.
  • Retrobulbar and peripheral capillary blood flow in hypercholesterolemic subjects
    Senn, B.; Orgül, S.; Keller, U.; Dickermann, D.; Dubler, B.; Vavrecka, J.; Gasser, P.; Kaiser, H.J.; Flammer, J.
  • Regional regulation of choroidal blood flow by autonomic innervation in the rat
    Steinle, J.J.; Krizsan-Agbas, D.; Smith, P.G.
  • Factors associated with long-term progression or stability in primary open-angle glaucoma
    Stewart, W.C.; Kolker, A.E.; Sharpe, E.D.; Day, D.G.; Holmes, K.T.; Leech, J.N.; Johnson, M.; Cantrell, J.B.
  • Association of endothelin-1 with normal tension glaucoma
    Sugiyama, T.; Moriya, S.; Oku, H.; Azuma, I.
  • Exploration of the role of reactive oxygen species in glutamate neurotoxicity in rat hippocampal neurones in culture
    Vergun, O.; Sobolevsky, A.I.; Yelshansky, M.V.; Keelan, J.; Khodorov, B.I.; Duchen, M.R.
  • Ocular blood flow measurement
    Williamson, T.H.; Harris, A.
  • Comparison of non-invasive methods for the assessment of haemodynamic drug effects in healthy male and female volunteers
    Wolzt, M.; Schmetterer, L.; Rheinberger, A.; Salomon, A.; Unfried, C.; Breiteneder, H.; Ehringer, H.; Eichler, H.G.; Fercher, A.F.
  • Measurement of microcirculation in the optic nerve head by laser speckle flowgraphy and scanning laser Doppler flowmetry
    Yaoeda, K.; Shirakashi, M.; Funaki, S.; Funaki, H.; Nakatsue, T.; Abe, H.
  • Measurement of microcirculation in optic nerve head by laser speckle flowgraphy in normal volunteers
    Yaoeda, K.; Shirakashi, M.; Funaki, S.; Funaki, H.; Nakatsue, T.; Fukushima, A.; Abe, H.

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