Purchase this article with an account.
H. Luan, R. Gupta, D. Pacheco, A. Seidner, J. Liggett, D.L. Knoerzer, J.R. Connor, Y. Ito, B. Berkowitz; Regulation of the Early Subnormal Retinal Oxygenation Response in Experimental Diabetes by Inducible Nitric Oxide Synthase . Invest. Ophthalmol. Vis. Sci. 2003;44(13):3902.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Purpose: To test the hypothesis that the inducible form of nitric oxide synthase (iNOS) contributes to the development of an early subnormal retinal oxygenation response in preclinical models of diabetic retinopathy. Methods: In urethane anesthetized Sprague Dawley rats or C57BL/6 mice, fMRI was used to noninvasively measure the change in retinal oxygen tension (ΔPO2) during a carbogen inhalation challenge. In the rat experiments, the retinal ΔPO2 of the following groups were compared: control rats (n = 9), 3 month diabetic rats (n = 5), and 3 month diabetic rats treated orally with L-N(6)-(1-iminoethyl)lysine 5-tetrazole amide, a prodrug of an inhibitor of inducible nitric oxide synthase (n = 6). In addition, the retinal ΔPO2 of the following mouse groups were compared: C57BL/6 mice (20), C57BL/6-Nos2tm1Lau mice (n = 10), 4 month diabetic mice (n = 13), and 4 month diabetic KO mice (n = 6). Results: The superior ΔPO2 of diabetic rats treated with the prodrug was not significantly (P > 0.05) different from their respective normal controls. In the mouse experiments, the superior retinal ΔPO2 of iNOS null mice was not statistically different (P > 0.05) from that of normal control mice. Only the ΔPO2 of the superior hemiretina of diabetic rat and mouse groups were significantly (P < 0.05) subnormal. Conclusions: iNOS is required for the development of an early subnormal ΔPO2 in experimental diabetic retinopathy.
This PDF is available to Subscribers Only