November 1993
Volume 34, Issue 12
Articles  |   November 1993
Resistance of diabetic rat electroretinogram to hypoxemia.
Author Affiliations
  • T Rimmer
    Department of Biomedical Engineering, Northwestern University, Evanston, Illinois 60208.
  • R A Linsenmeier
    Department of Biomedical Engineering, Northwestern University, Evanston, Illinois 60208.
Investigative Ophthalmology & Visual Science November 1993, Vol.34, 3246-3252. doi:
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      T Rimmer, R A Linsenmeier; Resistance of diabetic rat electroretinogram to hypoxemia.. Invest. Ophthalmol. Vis. Sci. 1993;34(12):3246-3252.

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      © ARVO (1962-2015); The Authors (2016-present)

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PURPOSE: To investigate the mechanisms of the known electroretinographic abnormalities of diabetic rats and to explore effects of hypoxemia. METHODS: Subretinal and vitreal microelectrodes were used to isolate the retinal and retinal pigment epithelial components of the electroretinogram. Normoxic and hypoxemic recordings were taken from nine normal and six streptozotocin-diabetic, anesthetized, paralyzed, and ventilated pigmented rats. RESULTS: When inspired O2 was reduced the retinal pigment epithelial c-wave component of most of the normal rats diminished, whereas those of the diabetic rats, though initially smaller, were more resistant to the episode of hypoxemia (P = 0.0061). A similar trend was seen in other components. CONCLUSION: It is proposed that the reduced sensitivity of the diabetic electroretinogram to hypoxemia results from a reduced dependency of the diabetic retina on oxygen. This reduced dependence may follow from a shift in adenosine triphosphate production whereby oxidative phosphorylation is reduced by the high level of retinal intracellular glucose (Crabtree effect). A reduced oxygen demand would cause a transient increase in retinal PO2, leading to a reduction in retinal blood flow. The resulting chronic hypoperfusion of the retinal circulation may deprive the retina of vital, non-energy-related substances.


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