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Martin Hammer, Tabitha Heller, Susanne Jentsch, Jens Dawczynski, Dietrich Schweitzer, Sven Peters, Ulrich A. Mueller; Retinal Vessel Oxygen Saturation Under Flicker Light Stimulation in Patients with Non-proliferative Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2011;52(14):5273.
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To investigate the response of retinal vessel diameters and oxygen saturation to flicker light stimulation of neuronal activity in patients with diabetic retinopathy.
18 patients with non-proliferative diabetic retinopathy (mean age: 62.2±8.3 years, diabetes type I/II: 4/14, HbA1c: 7.7±0.92, duration of diabetes: 24.1±9.3 years) and 20 healthy controls (71.2±7.5 years) were included. Dual - wavelength (548 nm and 610 nm) fundus images were taken before and during monochromatic (567 - 587 nm) luminance flicker stimulation (12.5 Hz, modulation depth: 1:20) for 90 s. Diameters (central retinal arterial and venous equivalents - CRAE and CRVE) and oxygen saturation (SO2, dual - wavelength optical oximetry) were determined and averaged for all arterioles and venules in an annular area centered at the optic disk ("ARIC" - grid). Changes of these parameters by the flicker were considered for statistical analysis.
Flicker light increased CRAE, CRVE, and venous SO2 by 1.42%±3.72%, 2.80%*±2.70%, and 2.03%*±2.43% in the patients as well as 4.98%*±6.23%, 8.94%*±5.26%, and 4.20%*±3.71% in the controls (*: p<0.05). This increase was significantly higher in the controls vs. patients for all parameters (t-test, p<0.05). The arterial SO2 remained unchanged in both groups. After adjustment for the subject’s age, the increase of the venous SO2 correlated significantly (p=0.035) with that of the CRAE in the controls but not in the diabetics.
Our results support the thesis of an impaired regulation of blood flow and oxygen supply to the diabetic retina. Whereas in healthy subjects the stimulation of neuronal activity increases the vascular diameters and, subsequently, the retinal blood flow and the venous oxygen saturation, this increase is reduced or totally abolished in diabetic retinopathy. This may hint at the role endothelial dysfunction in the etiology of the disease.
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