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T Abiko, A Abiko, N Horio, AC Clermont, BD Shoelson, GL King, SE Bursell; Microsphere Impaction and Retinal Hemodynamics . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1322.
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Purpose:Prior studies have shown that retinal mean circulation time (MCT) was prolonged and leukocyte entrapment (leukostasis) in retinal capillaries was increased in short duration diabetic rats. Leukostasis has been shown to be associated with localized capillary nonperfusion. Thus we investigated whether or not small particle retinal impaction could have a direct effect on retinal hemodynamics. Methods:Non-diabetic and streptozotocin-induced diabetic (1 week duration) Long-Evans rats were used. Fluorescent polystyrene microspheres (15µm diameter) were injected via the right carotid artery resulting in impactions only in right eye retinal vessels. The retinal images were recorded using the scanning laser ophthalmoscope (SLO) and MCT was measured using our video fluorescein angiography (VFA) methodology. The number of microspheres entering the eye was counted from the retinal video recordings. Two weeks later, VFA was performed to examine retinal microcirculation and measure MCTs from both eyes. Additionally the MCTs from both eyes were measured prior to microsphere injections to provide baseline comparison. Results:At baseline, there was no significant difference in MCTs comparing left and right eyes (1.03±0.15 and 1.06±0.13 sec, respectively). Microspheres appeared only in retinal arteries of right eyes, -and impacted only in the retinal arterioles and capillaries, but not the venules. In non-diabetic and diabetic rats there was no correlation (p=0.19, p=0.60, respectively) between the number of microspheres (0-1300) and relative MCT difference between right and left eyes. Conclusion:These results indicate that impactions at the numbers of microspheres had no significant direct effect on retinal hemodynamics suggesting that the observed retinal blood flow reductions and increased leukostasis in early diabetes were more likely to be related to the development of endothelial dysfunction in early diabetes.
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