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Editors Selection IGR 13-2

Visual function: Bloodflow

Comment by Alon Harris on:

11722 Enhanced endothelium derived hyperpolarising factor activity in resistance arteries from normal pressure glaucoma patients: implications for vascular function in the eye, Cleary C; Buckley CH; Henry E et al., British Journal of Ophthalmology, 2005; 89: 223-228

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Clinical studies have revealed ocular blood flow deficits in the retina, choroid and optic nerve tissues of glaucoma patients. Previous studies have reported reversible ocular vasospasm in patients with normal tension glaucoma (NTG).¹ While ocular hemodynamic deficits have been found in NTG patients, the metabolic regulation of ocular perfusion is complex and involves many physiochemical pathways, including that of nitric oxide (NO). When the metabolic demands of the retina rise, endothelial cells increase production of NO, resulting in vasodilatation of local ocular vasculature.^2,3 If the ocular autoregulation is abnormal as a result of dysfunctional NO production and/or utilization, the retina's metabolic needs may be compromised and apoptosis of retinal ganglion cells accelerated. Cleary et al. (180) have attempted to quantify endothelial cell dysfunction in patients with NTG by examining endothelium derived relaxing factor's effects on NTG patient's subcutaneous resistance arteries and porcine ciliary arteries. In NTG patients, inhibition of acetylcholine (ACh) mediated vascular relaxation by potassium channel antagonists (via endothelium derived hyperpolarizing factor (EDHF) inhibition) was significantly greater than in controls. Although controversial, the lack of effect of COX inhibition with meclofenamic acid in porcine arteries in this study supports some previous work suggesting prostaglandins do not contribute to ciliary vessel relaxation.

An increase of EDHF in response to decreased NO is suggested to be one pathway of the retina's ability to autoregulate blood flow. One limitation of this study is the small n of seven NTG patients and controls. The paper's emphasis on metabolic investigations, however, represents a vital step to our continued understanding of glaucomatous disease pathology. Ocular blood flow represents a surrogate for tissue oxygenation and toxin removal. In future research, endothelium derived relaxing factors should be evaluated in relation clinically to a patient's vision and measurable ocular perfusion. If EDHF and NO markers are indicative of tissue specific defects which can be assessed with current technologies, a greater differentiation of ischemic insult in glaucoma may be revealed.

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