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R.J. Casson, G. Chidlow, J.P. Wood, N.N. Osborne; Hyperglycemia Protects against Retinal Ischemia . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2933.
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Purpose: to investigate the effect of short-term experimental diabetes, systemic glucose delivery and intraocular glucose delivery on retinal ischemia. Methods: Prior to 45 or 60 minutes of pressure-induced retinal ischemia (using a 0.9% saline infusate), blood glucose levels (BGLs) were elevated in groups of age and sex matched Wistar rats by streptozotocin injection (5 days before) or i.p. glucose injection (20 minutes before). The electroretinogram was recorded 7 days post-ischemia, after which rats were killed for RT-PCR analysis or histopathology and compared to appropriate controls; other groups of rats received 60 minutes of pressure-induced ischemia using isotonic glucose, 2-deoxyglucose, or lactate as the intraocular infusate and underwent identical post-ischemia analysis. Results: After 45 minutes of ischemia, the b-wave amplitude was unchanged from baseline in hyperglycemics, compared to a 70% reduction in controls, and RT-PCR analysis showed a significantly greater loss of Thy-1 mRNA in the controls compared to the hyperglycemics. After 60 minutes of ischemia the b-wave amplitude still showed significantly greater preservation in the hyperglycemics compared to the controls, and the retinal morphology was remarkably preserved. Moderate hyperglycemia (BGLs 12-16mM produced the same degree of protection as severe hyperglycemia (BGL > 16.1mM). Isotonic glucose infusate also significantly preserved retinal structure and function, lactate infusate produced a similar degree of injury to the saline infusate, but 2-deoxyglucose infusate exacerbated the ischemic injury. Conclusion: Hyperglycemia and intraocular glucose delivery markedly attenuate ischemic retinal injury, a finding that may have important pathophysiological and clinical implications.
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