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P<P, published online ahead of print October 29, 2009
(Investigative Ophthalmology and Visual Science. )
© 2009 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.09-4191
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Hyperglycemia Rescues Retinal Neurons from Hypoperfusion-induced Injury

Matthew C Holman,1 Glyn Chidlow,2 John P Wood,3 and Robert J Casson4

1Ophthalmic Reseach Laboratories, South Australian Institute of Ophthalmology, Adelaide, Australia 2Ophthalmic Reseach Laboratories, South Australian Institute of Ophthalmology, Adelaide, Australia 3Ophthalmology Department, Royal Adelaide Hospital, Adelaide, Australia 4Ophthalmology, South Australian Institute of Ophthalmology, Adelaide, Australia

Correspondence: Matthew Holman, Email: holman.matthew{at}gmail.com

Abstract

Purpose: Due to differences in energy metabolism between the brain and retina, we hypothesized that in a model of ocular and cerebral hypoperfusion that retina would be protected by short-term hyperglycemia whilst the brain injury would be exacerbated.

Methods: Hyperglycemia was induced by intraperitoneal streptozotocin. An initial experiment determined the effect of hyperglycemia alone in sham-operated rats. Simultaneous retinal and cerebral hypoperfusion was achieved by 2-vessel occlusion (2VO; permanent ligation of both common carotid arteries). Hyperglycemia was induced 3 days prior to 2VO by streptozotocin injection. Rats were killed 7 days after 2VO or sham surgery. The retina of one eye was collected for histology/immunohistochemistry and the fellow retina was collected for real-time RT-PCR. Retinas were analysed for neuronal and glial markers and heat shock protein-27. Brains were processed for histology and immunohistochemistry.

Results: Short-term (approximately 10 days) hyperglycemia alone caused no discernible injury to the retina. Retinas of normoglycemic 2VO animals showed marked loss of retinal ganglion cells and horizontal cells, thinning of the inner retina, glial cell activation and infiltration of macrophages. Hyperglycemic 2VO rats displayed a remarkable protection of retinal structure and reduced glial cell activation compared to normoglycemic 2VO animals. There was significantly greater number of heat shock protein-27 positive retinal ganglion cells in normoglycemic animals compared to hyperglycemic animals. Brains of both normoglycemic and hyperglycemic 2VO animals displayed scattered ischemic infarcts and mild white matter injury.

Conclusions: Short-term hyperglycemia affords a robust protection against retinal hypoperfusion injury, but in the same animals brain injury is not ameliorated. The mechanism of this retinal hyperglycemiainduced neuroprotection requires further study.

Key Words: retinal ischemia • retinal metabolism • glaucoma • retinal blood flow






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