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M. Malmsjö, L. Gustafsson, B. Gesslein; Retinal Ischemia Reperfusion: A New Animal Model Suitable for Experimental Analysis of the Retinal Arteries. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3433.
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Identification of intracellular transduction pathways that are activated in retinal ischemia may be important to find new pharmacological targets to prevent retinal injury. Studies on retinal ischemia reperfusion have so far mainly focused on neuroprotective aspect of the problem. We believe that it is just as important to examine the changes in the vasculature that supply the retina with blood. Until now, most studies have been performed using rodents and smaller animals which lack retinal blood vessels that are adequate for experimental analysis. The aim of this study was to set up a porcine model for retinal ischemia reperfusion injury in order to make in detail studies on retinal arteries possible.
In each animal, ischemia was induced in one eye by raising the intraocular pressure above systolic blood pressure for one hour, while the other eye served as control. After 5, 12 or 20 hours of reperfusion the eye were enucleated and the retina and retinal arteries were studied. Tissue morphology and chromatin condensation was examined by microscopy using hematoxylin-eosin and the DNA specific dye TO-PRO-1 and pyknotic cell count. Glial fibrillary acidic protein (GFAP) mRNA expression was examined using quantitative real-time PCR.
Ophthalmologic inspection showed that when raising the intraocular pressure the blood flow in the retinal circulation was completely obliterated. The GFAP mRNA expression was increased after ischemia reperfusion (43±57% after 5 hours, 141±31% after 12 hours and 241±81% after 20 hours), which is a characteristic response after retinal injury. An increase in pyknotic nuclei count could be visualized using hematoxylin-eosin stained sections of the retina. TO-PRO-1 staining intensity was increased suggesting chromatin condensation in ischemia reperfusion (172±49% after 5 hours and 80±33% after 12 hours in the inner nuclear layer of the retina). Taken together, these results suggest that cell death is induced in this model of ischemia reperfusion.
This study is to our knowledge the first where ischemia reperfusion has been induced by elevating the intraocular pressure in a porcine eye. The basic structure of the porcine eye appears to have a typical primate-like architecture and is similar to the human eye regarding both the size and retinal blood supply. This porcine model of retinal ischemia reperfusion produces a substantial injury to the retinal tissue and as the size of the retinal arteries is similar to that in humans; this may be a suitable model for studying retinal circulatory failure.
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