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(Investigative Ophthalmology and Visual Science. 2003;44:1348-1354.)
© 2003 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.02-0368
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The Effect of Ischemic Preconditioning on Light-Induced Photoreceptor Injury

Robert J. Casson, John P. M. Wood, Jose Melena, Glyn Chidlow, and Neville N. Osborne

From the Nuffield Laboratory of Ophthalmology, Oxford University, Oxford, United Kingdom.

PURPOSE. To determine whether ischemic preconditioning (IPC) upregulates certain retinal survival factors and to assess the protective effect of retinal IPC against light-induced photoreceptor degeneration.

METHODS. Albino rats underwent IPC induced by raising the intraocular pressure in one eye to 120 mm Hg for 5 minutes. The fellow eye underwent sham treatment. Basic fibroblast growth factor (bFGF), ciliary neurotrophic factor (CNTF), brain-derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), and Bcl-2 were measured after 6 and 48 hours, by the reverse transcription-polymerase chain reaction and immunoblot analysis. Other preconditioned rats received 48 hours of photic injury (2000 lux) 24 hours after IPC. The a- and b-wave amplitudes of the flash electroretinograms were measured 5 days later, followed by analysis of rhodopsin mRNA levels and histology. The influence of adenosine A1 receptor blockade was assessed.

RESULTS. bFGF, GFAP, and Bcl-2 were upregulated after IPC. BDNF was not upregulated. The marked reduction of the a- and b-wave amplitudes and the structural injury to the photoreceptors induced by the photic insult were significantly reduced by IPC. The protection afforded by IPC was not influenced by adenosine A1 antagonism.

CONCLUSIONS. IPC upregulates bFGF, GFAP, and Bcl-2 and protects photoreceptors against light-induced injury. These factors may be involved in the protective response.




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