title: Vasospasm in glaucoma: clinical and laboratory aspects.
abstract: During the last decade, the presumed etiology of glaucoma has moved from a pure pressure concept to a combined mechanical and vascular theory. Evidence of a localized vascular insufficiency leading to perfusion deficits of ocular structures, including the optic nerve head, the retina, the choroid, and the retrobulbar vessels, is now clear. This article evaluates the role of vasospasm as the primary cause of such a vascular failure. The role of both ocular and systemic vasospasms and their clinical correlations are discussed. At a cellular level, the function of the modulating role of the vascular endothelium is reviewed. Evidence of abnormalities of the vascular endothelium and its vasoactive peptides as a conduit for vasospasm is mounting. Herein lies exciting prospects for potential pharmacologic targets in future glaucoma management.
authors.affiliation: Mater Misericordiae Hospital, Dublin, Ireland.
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Delaney
authors.forename: Tony E
authors.initials: TE
authors.lastname: Walshe
authors.forename: Colm
authors.initials: C
authors.lastname: O'Brien
mesh_terms: D001783:Blood Flow Velocity; D019332:Endothelin-1 / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D005123:Eye / Q000098:blood supply; D005902:Glaucoma, Open-Angle / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism; D009880:Ophthalmic Artery / Q000503:physiopathology*; D014661:Vasoconstriction / Q000502:physiology*
chemical_list: D019332:Endothelin-1; D009569:Nitric Oxide