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Florian Wabnig, Daniel Schroeder, Maria Guschlbauer, Tim Hucho, Konrad R Koch, Claus Cursiefen, Ludwig M Heindl; Effect of global ischemia/reperfusion on the retina in a rat model of cardiac arrest. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):183.
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© ARVO (1962-2015); The Authors (2016-present)
Global ischemia/reperfusion as encountered following resuscitation leads to a generalized inflammatory reaction (“post-cardiac-arrest syndrome”). Neuronal cell death in selectively vulnerable areas of the brain has been observed. Local retinal ischemia has extensively been studied, however, effects of global ischemia on the retina and underlying pathologic mechanisms have not been analyzed yet. Therefore, we studied morphological changes in the retina in a rat model of resuscitation.
Male adult Wistar rats were anaesthetized and cardiac arrest was induced via an esophageal electrode using alternating current (12V, 50Hz). After 6 minutes, cardiopulmonary resuscitation was performed. Animals reaching return of spontaneous circulation (ROSC) within 5 minutes were followed for different periods of time (24h, 72h and 14 days post ROSC), after which they were euthanized, eyes were enucleated and paraffin-embedded (n=2 per time point). Three sections per eye, each containing the optic nerve, were stained for hematoxylin&eosin, and the retina was examined at 3 different locations (equatorial, midperipheral, parapapillary). Ganglion cell complex thickness (GCCT), total retinal thickness (TRT), number of retinal ganglion cells (RGC), cell body layers of the inner (INL) and outer nuclear layers (ONL) were measured and compared to untreated controls.
In the equatorial plane no significant differences could be observed (GCCT, p=0.211; TRT, p=0.617; RGC number, p=0.264; cell body layers in INL, p=0.351; cell body layers in ONL, p=0.454). In the midperipheral plane no significant differences could be seen (GCCT, p=0.133; TRT, p=0.484; RGC number, p=0.264; cell body layers in INL, p=0.902; cell body layers in ONL, p=0.257). In the parapapillary plane no significant differences could be detected (GCCT, p=0.945; TRT, p=0.077; RGC number, p=0.718; cell body layers in INL, p=0.446; cell body layers in ONL, p=0.211).
Our results could not reveal any changes in retinal morphology following global ischemia/reperfusion. Further evaluation of possible retinal changes including other time points as well as immunohistological examinations will be needed. Nevertheless, the presented model allows for studying the impact of global retinal ischemia/ischemia reperfusion on the eye in detail.
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