Introductory comments for session V "neovasculogenesis" presented at the fifth symposium, the International Society on Metabolic Eye Disease October 24-26, 1982.
Physiopathologic or metabolic alterations in retinal blood vessels resulting in an ischemic state may be a prime trigger mechanism in neovasculogenesis and scar tissue formation. Rate of oxygen delivery may be the primary factor so the end-state disease may be rapid as in retrolental fibroplasia (marked reduction in vascular flow due to acute vasoconstriction) or delayed as in diabetes mellitus (chronic metabolism-induced low oxygen release rates parallel with chronic vasodilation).
D000818:Animals; D003930:Diabetic Retinopathy / Q000209:etiology / Q000378:metabolism; D004285:Dogs; D005123:Eye / Q000098:blood supply*; D006801:Humans; D007511:Ischemia / Q000150:complications; D009389:Neovascularization, Pathologic / Q000503:physiopathology; D010101:Oxygen Consumption; D011453:Prostaglandins / Q000502:physiology; D012178:Retinopathy of Prematurity / Q000209:etiology / Q000378:metabolism; D014661:Vasoconstriction; D014664:Vasodilation
D011453:Prostaglandins