IOVS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rimmer, T.
Right arrow Articles by Linsenmeier, R. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rimmer, T.
Right arrow Articles by Linsenmeier, R. A.

Investigative Ophthalmology & Visual Science, Vol 34, 3246-3252, Copyright © 1993 by Association for Research in Vision and Ophthalmology

ARTICLES AND REPORTS

Resistance of diabetic rat electroretinogram to hypoxemia

T Rimmer and RA Linsenmeier
Department of Biomedical Engineering, Northwestern University, Evanston, Illinois 60208.

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.


This article has been cited by other articles:


Home page
 DiabetesHome page
J. R. Nyengaard, Y. Ido, C. Kilo, and J. R. Williamson
Interactions Between Hyperglycemia and Hypoxia: Implications for Diabetic Retinopathy
Diabetes, November 1, 2004; 53(11): 2931 - 2938.
[Abstract] [Full Text] [PDF]

Home page
 Arch OphthalmolHome page
R. J. Casson, G. Chidlow, J. P. M. Wood, and N. N. Osborne
The Effect of Hyperglycemia on Experimental Retinal Ischemia
Arch Ophthalmol, March 1, 2004; 122(3): 361 - 366.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
L. Padnick-Silver and R. A. Linsenmeier
Effect of Acute Hyperglycemia on Oxygen and Oxidative Metabolism in the Intact Cat Retina
Invest. Ophthalmol. Vis. Sci., February 1, 2003; 44(2): 745 - 750.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1993 by the Association for Research in Vision and Ophthalmology