Increased intraretinal PO2 in short-term diabetic rats

  1. Robert A. Linsenmeierb,c,d,*
  1. aDepartment of Chemical and Biological Engineering, Northwestern University, Evanston, IL 60208, USA
  2. Departments of bBiomedical Engineering and
  3. cNeurobiology, Northwestern University, Evanston, IL 60208, USA and
  4. dDepartment of Ophthalmology, Northwestern University, Chicago, IL, USA
  1. *Corresponding author: Robert A. Linsenmeier, E-mail: r-linsenmeier{at}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 VEGF levels increased. At 12 weeks, average inner retinal PO2, normalized to choriocapillaris PO2, was higher in diabetics 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.

  • Received January 19, 2014.
  • Accepted July 11, 2014.

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