March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Retinal Neuroprotection Against Ischemia/Reperfusion Damage Induced By Global And Local Hypothermia
Author Affiliations & Notes
  • Ezequiel M. Salido
    Human Biochemistry, University of Buenos Aires (UBA), CABA, Argentina
  • Damian Dorfman
    Human Biochemistry, University of Buenos Aires (UBA), CABA, Argentina
  • Monica Chianelli
    Human Biochemistry, University of Buenos Aires (UBA), CABA, Argentina
  • Ruth E. Rosenstein
    Human Biochemistry, University of Buenos Aires (UBA), CABA, Argentina
  • Footnotes
    Commercial Relationships  Ezequiel M. Salido, None; Damian Dorfman, None; Monica Chianelli, None; Ruth E. Rosenstein, None
  • Footnotes
    Support  CONICET / UBA / ANPCyT
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 5326. doi:https://doi.org/
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      Ezequiel M. Salido, Damian Dorfman, Monica Chianelli, Ruth E. Rosenstein; Retinal Neuroprotection Against Ischemia/Reperfusion Damage Induced By Global And Local Hypothermia. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5326. doi: https://doi.org/.

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

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Abstract
 
Purpose:
 

Retinal ischemia could provoke blindness. There is no effective treatment against retinal ischemic damage. We investigated whether a brief global or local hypothermia could induce ischemic tolerance in the rat retina.

 
Methods:
 

Ischemia was induced in male Wistar rats by increasing intraocular pressure to 140 mm Hg for 50 minutes. One day before ischemia, animals underwent a 20-minute period of hypothermia by lowering the whole body temperature to 32ºC or by cooling only one eye to 32ºC for 30 min. Two weeks after ischemia, animals were subjected to electroretinography (ERG) and histological analysis. Moreover, glutamate uptake was assessed using 3H-glutamate, and glutamine synthetase activity was assessed by a spectrophotometric assay.

 
Results:
 

Retinal ischemia induced a significant decrease in oscillatory potentials, and scotopic ERG a- and b-wave amplitude, which was significantly prevented by global or monocular hypothermia. Retinal ischemia induced a significant decrease in glutamate uptake and glutamine synthetase activity, whereas monocular hypothermia prevented the effect of ischemia on glutamate recycling. The intravitreal injection of supraphysiological concentrations of glutamate mimicked electroretinographic and histological alterations provoked by ischemia, which were significantly abrogated by hypothermic preconditioning.

 
Conclusions:
 

These results indicate that hypothermia significantly protected retinal function and histology against ischemia/reperfusion injury. Hypothermic preconditioning could provide a relatively low-risk approach for treating retinal ischemic pathologies.

 
Keywords: neuroprotection • ischemia • electroretinography: non-clinical 
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