Flicker Light–Induced Retinal Vasodilation in Diabetes and Diabetic Retinopathy

نویسندگان

  • Thanh T. Nguyen
  • Ryo Kawasaki
  • Jie Jin Wang
  • Andreas J. Kreis
  • Jonathan Shaw
  • Walthard Vilser
  • Tien Y. Wong
چکیده

OBJECTIVE Flicker light-induced retinal vasodilation may reflect endothelial function in the retinal circulation. We investigated flicker light-induced vasodilation in individuals with diabetes and diabetic retinopathy. RESEARCH DESIGN AND METHODS Participants consisted of 224 individuals with diabetes and 103 nondiabetic control subjects. Flicker light-induced retinal vasodilation (percentage increase over baseline diameter) was measured using the Dynamic Vessel Analyzer. Diabetic retinopathy was graded from retinal photographs. RESULTS Mean +/- SD age was 56.5 +/- 11.8 years for those with diabetes and 48.0 +/- 16.3 years for control subjects. Mean arteriolar and venular dilation after flicker light stimulation were reduced in participants with diabetes compared with those in control subjects (1.43 +/- 2.10 vs. 3.46 +/- 2.36%, P < 0.001 for arteriolar and 2.83 +/- 2.10 vs. 3.98 +/- 1.84%, P < 0.001 for venular dilation). After adjustment for age, sex, diabetes duration, fasting glucose, cholesterol and triglyceride levels, current smoking status, systolic blood pressure, and use of antihypertensive and lipid-lowering medications, participants with reduced flicker light-induced vasodilation were more likely to have diabetes (odds ratio 19.7 [95% CI 6.5-59.1], P < 0.001 and 8.14 [3.1-21.4], P < 0.001, comparing lowest vs. highest tertile of arteriolar and venular dilation, respectively). Diabetic participants with reduced flicker light-induced vasodilation were more likely to have diabetic retinopathy (2.2 [1.2-4.0], P = 0.01 for arteriolar dilation and 2.5 [1.3-4.5], P = 0.004 for venular dilation). CONCLUSIONS Reduced retinal vasodilation after flicker light stimulation is independently associated with diabetes status and, in individuals with diabetes, with diabetic retinopathy. Our findings may therefore support endothelial dysfunction as a pathophysiological mechanism underlying diabetes and its microvascular manifestations.

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عنوان ژورنال:

دوره 32  شماره 

صفحات  -

تاریخ انتشار 2009