Abstract
Retinal ischemia could provoke blindness. At present, there is no effective treatment against retinal ischemic damage. Strong evidence supports that glutamate is implicated in retinal ischemic damage. We investigated whether a brief period of global or ocular hypothermia applied 24 h before ischemia (i.e. hypothermic preconditioning, HPC) protects the retina from ischemia/reperfusion damage, and the involvement of glutamate in the retinal protection induced by HPC. For this purpose, ischemia was induced by increasing intraocular pressure to 120 mm Hg for 40 min. One day before ischemia, animals were submitted to global or ocular hypothermia (33°C and 32°C for 20 min, respectively) and fourteen days after ischemia, animals were subjected to electroretinography and histological analysis. Global or ocular HPC afforded significant functional (electroretinographic) protection in eyes exposed to ischemia/reperfusion injury. A marked alteration of the retinal structure and a decrease in retinal ganglion cell number were observed in ischemic retinas, whereas global or ocular HPC significantly preserved retinal structure and ganglion cell count. Three days after ischemia, a significant decrease in retinal glutamate uptake and glutamine synthetase activity was observed, whereas ocular HPC prevented the effect of ischemia on these parameters. The intravitreal injection of supraphysiological levels of glutamate induced alterations in retinal function and histology which were significantly prevented by ocular HPC. These results support that global or ocular HPC significantly protected retinal function and histology from ischemia/reperfusion injury, probably through a glutamate-dependent mechanism.
Highlights
Retinal ischemia plays a key role in some of the most common blinding diseases, such as diabetic retinopathy, glaucoma, retinal vascular occlusions, and retinopathy of prematurity, among others
Faberowski et al [21] demonstrated a significant neuroprotection of local hypothermia in a ligation-induced I/R model in the rat retina, and the protective effect of lowering body temperature during retinal ischemia has been observed in high intraocular pressure models in rabbit and mouse [22,23]
Global hypothermic preconditioning (HPC) significantly prevented the decrease in ERG a- and b-wave amplitude induced by I/R
Summary
Retinal ischemia plays a key role in some of the most common blinding diseases, such as diabetic retinopathy, glaucoma, retinal vascular occlusions, and retinopathy of prematurity, among others. Faberowski et al [21] demonstrated a significant neuroprotection of local hypothermia in a ligation-induced I/R model in the rat retina, and the protective effect of lowering body temperature during retinal ischemia has been observed in high intraocular pressure models in rabbit and mouse [22,23]. Lowering body temperature to 33uC during ischemia and reperfusion in the retina markedly reduces ischemia-induced cell loss in the ganglion cell layer (GCL) [24] These results indicate that intraischemic hypothermia limits retinal ischemic damage, the efficacy of HPC against retinal I/R injury was not previously examined. The aim of the present study was to analyze the capacity of a short period of global or ocular hypothermia applied before the ischemic event, for protecting the retinal function and histology against I/R damage
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