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No‐induced retinal vasodilatation is maintained in type 1 diabetes
Author(s) -
PEMP B,
GARHOFER G,
WEIGERT G,
KARL K,
WOLZT M,
SCHMETTERER L
Publication year - 2008
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2008.6443.x
Subject(s) - retinal , vasodilation , medicine , diabetes mellitus , autoregulation , diabetic retinopathy , retina , perfusion , blood pressure , cardiology , vasoconstriction , retinopathy , ophthalmology , endocrinology , biology , neuroscience
Purpose Various studies have shown that retinal vessels in patients with diabetes mellitus have a reduced capacity to adapt to changes of perfusion pressure. The mechanisms lying behind this abnormal autoregulation have not been completely identified yet. Histomorphological changes of retinal vessels in diabetes could possibly reduce their capacity of vasodilation and vasoconstriction. To test this hypothesis we compared the response of retinal vessel diameters to systemic glyceryl trinitrate (GTN) in patients with diabetes and healthy controls. Methods 20 patients with insulin dependent diabetes mellitus featuring no or mild non‐proliferative diabetic retinopathy were included into this study. In addition, 20 healthy and age‐matched subjects were included as controls. Retinal vessel diameters were measured before and immediately after sublingual application of 0.8 mg of the NO‐donor GTN. The IMEDOS Retinal Vessel Analyzer was used for continuous measurement of diameters of retinal arteries and veins. Results Oral application of GTN induced vasodilatation of retinal arteries and veins. This effect was not different between patients with diabetes and healthy controls. Systemic arterial blood pressure was reduced in both groups after GTN application, but to a comparable degree. Conclusion The present study indicates that in patients with no or mild non‐proliferative diabetic retinopathy the vasodilatory response of retinal vessels to a direct NO‐donor is maintained. This indicates that abnormal retinal autoregulation in diabetes mellitus, as observed previously, is not a consequence of generally reduced retinal vascular reactivity.