Abstract

Glaucoma, a common cause of blindness worldwide, is characterized by an increasing visual field loss and a characteristic excavation of the optic nerve head. Increased intraocular pressure (IOP) is one main risk factor for glaucoma, yet there is increasing evidence that other risk factors are involved in the development of glaucoma, such as impaired ocular blood flow and oxidative stress.^1-3^ On the average, blood flow is reduced in glaucoma patients. It is particularly reduced in patients with normal tension glaucoma as well as in patients with high tension glaucoma who progress despite a normalized IOP. A constant reduction of blood flow as commonly seen in patients with a secondary vascular dysregulation, can lead to atrophy but does not contribute to glaucomatous atrophy. An instability of ocular blood flow however, is clearly linked to occurrence and progression of glaucomatous optic neuropathy. Ocular blood flow is unstable, if IOP fluctuates on a high enough or blood pressure on a low enough level to temporarily exceed the capacity of autoregulatory mechanisms. Ocular blood flow is however also reduced if autoregulation itself is disturbed. Reduced autoregulation occurs particularly in patients suffering from the Flammer-Syndrome. Instability of blood flow (unstable oxygen supply to the optic nerve) leads to oxidative stress, which in turn, leads to the production of peroxynitrite (ONOO-) leading to death of ganglion cells. This article summarizes the importance of ocular blood flow and oxidative stress for the pathogenesis of glaucoma.

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