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B.A. Berkowitz, H. Luan, Y. Ito, B. Winkler, C.A. Starnes, R. Roberts; Subnormal Retinal Oxygenation Response in: Experimental Diabetic Retinopathy: Metabolic or Vasoregulatory Mechanism? . Invest. Ophthalmol. Vis. Sci. 2005;46(13):400.
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Purpose:To test the hypothesis that subnormal retinal ΔPO2 associated with experimental diabetes is a measure of alterations in retinal oxygen supply regulation and not retinal metabolism. Methods: In separate groups of age–matched control (C) and diabetic (D) rats, preretinal vitreous PO2 measurements were made using 19F NMR and a perfluorocarbon droplet (0.3 µl) during room air or 12% oxygen breathing, retinal ATP, lactate, NAD, and NADH levels were measured biochemically, and retinal oxygenation responses were measured during room air and a 4 min carbogen challenge to generate retinal ΔPO2 between the initial room air and carbogen conditions and the two carbogen conditions. Results: Significant (P < 0.05) preretinal hypoxia was found in control rats breathing 12% oxygen compared with room air. No significant differences (P > 0.05) were found in preretinal PO2 or retinal ATP, lactate, NAD, and NADH levels between C and D rats. In C and D rats, inferior hemiretinal ΔPO2 were not different (P > 0.05) at any time. As expected, during the first 2 min on carbogen, diabetic superior hemiretinal ΔPO2 was 43% subnormal compared with controls (P < 0.05). In contrast, the superior hemiretinal ΔPO2 measured using the first and second images collected during carbogen breathing for the control group was 41% less (P < 0.05) than that for the diabetic group. Conclusions: The lack of a difference in baseline oxygen levels and energy–related enzyme concentrations up to 13 mo of diabetes, and the different temporal evolution of the retinal oxygenation response in control and diabetic rats support our working hypothesis.
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