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Line Petersen, Toke Bek; The diameter of retinal arterioles in diabetic maculopathy is unaffected by hypoxia and inhibition of NO and COX synthesis. Invest. Ophthalmol. Vis. Sci. 2016;57(12):4593.
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© ARVO (1962-2015); The Authors (2016-present)
Diabetic retinopathy (DR) is characterized by a number of changes in retinal physiology including impaired diameter regulation of retinal arterioles and retinal hypoxia. Previous studies of normal persons and diabetic patients without DR have shown that hypoxia-induced vasodilatation is mediated by cyclo-oxygenase (COX) and nitric oxide (NO). The purpose of the present study was to study whether these effects are preserved in patients with diabetic maculopathy.
Eighteen patients with diabetic maculopathy aged 29-57 years were examined using the Dynamic Vessel Analyzer. The resting diameter and the diameter changes secondary to isometric exercise and flicker stimulation of retinal arterioles were measured before and during breathing a hypoxic gas mixture of 12.5 % oxygen/87.5 % nitrogen. The examinations were performed before and during intravenous infusion of the NOS inhibitor L-NMMA and were repeated on a second day after topical administration of the COX-inhibitor diclofenac.
Hypoxia induced no significant change in the diameter of retinal arterioles, and the diameter showed no significant change in response to L-NMMA infusion or topical application of diclofenac (p>0.25 for all comparisons) and no significant change in response to isometric exercise or flicker light stimulation (p>0.05).
Hypoxia-induced vasodilatation is severely reduced in patients with diabetic maculopathy. Future intervention studies aimed at normalizing the diameter regulation of retinal arterioles in diabetic patients should preferentially be conducted in the early stages of the disease where the potential for changing the vessel diameter is preserved.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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