Musa Yasin Kaya1, Line Petersen2, Toke Bek2. 1. Department of Ophthalmology, Aarhus University Hospital, DK-8000, Aarhus C, Denmark. musa.yasin.kaya@post.au.dk. 2. Department of Ophthalmology, Aarhus University Hospital, DK-8000, Aarhus C, Denmark.
Abstract
PURPOSE: Retinal hypoxia with consequent changes in blood flow play a role in a number of vision-threatening diseases, such as diabetic retinopathy. Previous studies have shown that the inhibition of nitric oxide synthase (NOS) and cyclooxygenase (COX) products are involved in the diameter regulation of the retinal vessels during hypoxia. Therefore, the aim of the present study was to examine the effects of an NO donor combined with COX inhibition on the diameter regulation of retinal vessels during hypoxia in normal persons. METHODS: Twenty normal persons aged 21-47 years were examined. The Dynamic Vessel Analyzer (DVA) was used to measure retinal vessel diameters at rest, during isometric exercise, and during flicker stimulation. The measurements were performed during normoxia and hypoxia before and after sublingual administration of the NO donor nitroglycerin, and were repeated on a second study day after topical administration of the COX-inhibitor diclofenac. RESULTS: The resting diameter of arterioles and venules increased significantly during hypoxia (p < 0.0001). Hypoxia also significantly reduced the arteriolar constriction during isometric exercise, and the dilatation of the arterioles and venules during flicker stimulation (p < 0.0001). Diclofenac further reduced the arteriolar constriction induced by isometric exercise during hypoxia (p = 0.005). However, the NO-donor nitroglycerin had no effect on vascular diameters. CONCLUSION: Diameter regulation of retinal vessels during hypoxia in normal persons can be influenced by the inhibition of COX products, but not by increasing the NO concentration. The findings suggest that the vasoactive effects of NO on retinal arterioles during hypoxia are saturated in normal persons.
PURPOSE:Retinal hypoxia with consequent changes in blood flow play a role in a number of vision-threatening diseases, such as diabetic retinopathy. Previous studies have shown that the inhibition of nitric oxide synthase (NOS) and cyclooxygenase (COX) products are involved in the diameter regulation of the retinal vessels during hypoxia. Therefore, the aim of the present study was to examine the effects of an NO donor combined with COX inhibition on the diameter regulation of retinal vessels during hypoxia in normal persons. METHODS: Twenty normal persons aged 21-47 years were examined. The Dynamic Vessel Analyzer (DVA) was used to measure retinal vessel diameters at rest, during isometric exercise, and during flicker stimulation. The measurements were performed during normoxia and hypoxia before and after sublingual administration of the NO donornitroglycerin, and were repeated on a second study day after topical administration of the COX-inhibitor diclofenac. RESULTS: The resting diameter of arterioles and venules increased significantly during hypoxia (p < 0.0001). Hypoxia also significantly reduced the arteriolar constriction during isometric exercise, and the dilatation of the arterioles and venules during flicker stimulation (p < 0.0001). Diclofenac further reduced the arteriolar constriction induced by isometric exercise during hypoxia (p = 0.005). However, the NO-donornitroglycerin had no effect on vascular diameters. CONCLUSION: Diameter regulation of retinal vessels during hypoxia in normal persons can be influenced by the inhibition of COX products, but not by increasing the NO concentration. The findings suggest that the vasoactive effects of NO on retinal arterioles during hypoxia are saturated in normal persons.
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