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Diabetes. 2014 Dec;63(12):4338-42. doi: 10.2337/db14-0101. Epub 2014 Jul 15.

Increased intraretinal PO2 in short-term diabetic rats.

Author information

1
Department of Chemical and Biological Engineering, Northwestern University, Evanston, IL.
2
Department of Biomedical Engineering, Northwestern University, Evanston, IL Department of Neurobiology, Northwestern University, Evanston, IL Department of Ophthalmology, Northwestern University, Chicago, IL r-linsenmeier@northwestern.edu.

Abstract

In diabetic retinopathy, neovascularization is hypothesized to develop due to hypoxia in the retina. However, evidence for retinal hypoxia is limited, and the progressive changes in oxygenation are unknown. The objective of this study was to determine if retinal hypoxia occurs early in the development of diabetes. Intraretinal oxygen (PO2) profiles were recorded with oxygen-sensitive microelectrodes in control and diabetic Long-Evans rats at 4 and 12 weeks after induction of diabetes. Diabetes did not affect oxygen consumption in the photoreceptors in either dark or light adaptation. Oxygenation of the inner retina was not affected after 4 weeks of diabetes, although vascular endothelial growth factor levels increased. At 12 weeks, average inner retinal PO2, normalized to choriocapillaris PO2, was higher in diabetic rats than in age-matched controls, which was opposite to what was expected. Thus retinal hypoxia is not a condition of early diabetes in rat retina. Increased inner retinal PO2 may occur because oxygen consumption decreases in the inner retina.

PMID:
25028524
PMCID:
PMC4238003
DOI:
10.2337/db14-0101
[Indexed for MEDLINE]
Free PMC Article

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