To determine the effect of hyperglycemia and intraocular glucose deliveryon ischemic retinal injury.
Experimental diabetes was induced in age- and sex-matched Wistar ratsby an injection of streptozocin. The functional and structural retinal injuryin these rats after a period of pressure-induced retinal ischemia was comparedwith the injury in appropriate controls and with rats made hyperglycemic byan injection of systemic glucose. The effect of high intraocular pressure–inducedischemia with the use of several different isotonic substrates in the elevatedreservoir (isotonic sodium chloride solution, glucose, 2-deoxyglucose, andlactate) was also determined. Electroretinography, reverse transcriptase polymerasechain reaction, and histologic examination were used to assess the retinalinjury.
Streptozocin-induced diabetes, glucose injection–induced preexistinghyperglycemia, and intraocular glucose delivery during ischemia markedly reducedthe functional and structural ischemic retinal injury. Neither postischemichyperglycemia nor the intraocular delivery of lactate significantly affectedthe ischemic injury; however, the intraocular delivery of 2-deoxyglucose significantlyexacerbated the retinal injury.
Preexisting hyperglycemia and the intraocular delivery of glucose markedlyattenuate ischemic retinal injury.
These findings highlight fundamental differences in energy metabolismbetween brain and retina, have important implications for the pathophysiologyof diabetic retinopathy, and may lead to novel therapeutic strategies forischemic retinopathies.