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Moe H. Aung, Moon K. Kim, Peter M. Thule, Machelle T. Pardue; Assessing Flicker-induced Retinal Vascular Responses using Scanning Laser Ophthalmoscope. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5434.
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© ARVO (1962-2015); The Authors (2016-present)
Flicker-induced vasodilation, also known as functional hyperemia, is a hemodynamic response that increases retinal blood flow to match neuronal activity. Recent studies have demonstrated a reduction in this response in patients with diabetes but without retinopathy. By limiting nutrient delivery during periods of increased neuronal activity, dysregulation of functional hyperemia may impair retinal function. Diminished vasodilation response has been observed in explanted retinae of rats kept hyperglycemic for five months. We asked if shorter durations of hyperglycemia could impair functional hyperemia and if this deficit could be assessed in vivo.
At 1.5 months of age, pigmented Long-Evans rats were randomly divided into two groups: control (n=6) and diabetic (n=8, induced by 100mg/kg streptozotocin (STZ) injection). Diabetes was confirmed by serially elevated blood glucose (>250mg/dL). Functional hyperemic response in the arteriole (induced by 530nm light flickering at 12Hz) and unchallenged arteriolar caliber of each rat were obtained at baseline, 2-week, and 6-week of hyperglycemia using a commercially available scanning laser ophthalmoscope (SLO) and analyzed offline with an imaging software. Only responses from the right eye were analyzed and compared between the two groups.
Baseline arteriolar functional hyperemic response was similar between control and diabetic rats, averaging 11.82 ± 2.77% (Mean ± SEM). Moreover, diabetic rats exhibited a tendency toward a reduced response (~8%) when compared to control rats at 2-wk post-STZ (p=0.062). However, this deficit was not sustained at 6-wk post-STZ. Under unchallenged conditions, retinal arterioles of diabetic rats were slightly more dilated than the controls at both 2-wk (6.61%) and 6-wk (6.74%) post-STZ, though the differences were not statistically significant.
We were able to assess flicker-induced vascular response using a commercially available SLO apparatus in vivo. As a proof of principle, we were able to monitor this response in a Type I diabetic rat model and found that diabetic rats had marginally significant deficit in this response as early as 2-wk post-STZ. This preparation will allow us to further characterize the mechanisms mediating defective functional hyperemia in early-stage diabetic retinopathy and assess the therapeutic success in rectifying this deficit in vivo.
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