Purchase this article with an account.
Norman P. Blair, Justin M. Wanek, Marek Mori, Mahnaz Shahidi; Abnormal Retinal Vascular Oxygen Tension Response to Light Flicker in Diabetic Rats. Invest. Ophthalmol. Vis. Sci. 2009;50(11):5444-5448. doi: 10.1167/iovs.09-3465.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To test the hypothesis that the intravascular oxygen response to light flicker is abnormal in diabetes.
Ten eyes of normal rats and 10 eyes of rats made diabetic with streptozotocin were examined. Oxygen tension (Po 2) was measured noninvasively in the retinal arteries and veins on optical section retinal images. Po 2 was estimated based on the quenching by oxygen of the phosphorescence of an intravenously injected palladium porphyrin molecular probe. Measurements were conducted with and without light flicker at 10 Hz. Oxygen saturation (So 2) was calculated with adjustment for the arterial pH.
In the normal rats flicker induced an increase in arterial Po 2 and in the difference in arterial and venous (A-V difference) Po 2 from 51 ± 5 (mean and SD) to 55 ± 7 mm Hg and from 22 ± 3 to 26 ± 5 mm Hg, respectively (P < 0.002 and 0.015, respectively). Flicker induced an increase of arterial So 2 and A-V So 2 difference from 64% ± 8% to 68% ± 7% and from 34% ± 4% to 38% ± 6%, respectively (P < 0.002 and 0.035, respectively). No changes in Po 2 or So 2 were observed with flicker in the veins. In the diabetic rats, no significant flicker-induced changes were seen in Po 2 or So 2 in the retinal arteries, veins, or A-V differences.
The diabetic rats lacked the flicker induced increase in arterial Po 2 and So 2 and also the A-V difference in Po 2 and So 2 observed in the normal rats. The best explanation appeared to be that diabetes impairs the increase in oxygen consumption normally provoked by light flicker.
This PDF is available to Subscribers Only