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Short-Time Ocular Ischemia Induces Vascular Endothelial Dysfunction and Ganglion Cell Loss in the Pig Retina.

Sciprofile linkJenia Kouchek Zadeh, Sciprofile linkAndreas Garcia-Bardon, Sciprofile linkErik K. Hartmann, Sciprofile linkNorbert Pfeiffer, Sciprofile linkWael Omran, Sciprofile linkM. Ludwig, Sciprofile linkAndreas Patzak, Sciprofile linkNing Xia, Sciprofile linkHuige Li, Sciprofile linkAdrian Gericke
Published: 21 September 2019
 by  MDPI
International Journal of Molecular Sciences , Volume 20; doi:10.3390/ijms20194685

Abstract: Visual impairment and blindness are often caused by retinal ischemia-reperfusion (I/R) injury. We aimed to characterize a new model of I/R in pigs, in which the intraocular pathways were not manipulated by invasive methods on the ocular system. After 12 min of ischemia followed by 20 h of reperfusion, reactivity of retinal arterioles was measured in vitro by video microscopy. Dihydroethidium (DHE) staining, qPCR, immunohistochemistry, quantification of neurons in the retinal ganglion cell layer, and histological examination was performed. Retinal arterioles of I/R-treated pigs displayed marked attenuation in response to the endothelium-dependent vasodilator, bradykinin, compared to sham-treated pigs. DHE staining intensity and messenger RNA levels for HIF-1α, VEGF-A, NOX2, and iNOS were elevated in retinal arterioles following I/R. Immunoreactivity to HIF-1α, VEGF-A, NOX2, and iNOS was enhanced in retinal arteriole endothelium after I/R. Moreover, I/R evoked a substantial decrease in Brn3a-positive retinal ganglion cells and noticeable retinal thickening. In conclusion, the results of the present study demonstrate that short-time ocular ischemia impairs endothelial function and integrity of retinal blood vessels and induces structural changes in the retina. HIF-1α, VEGF-A, iNOS, and NOX2-derived reactive oxygen species appear to be involved in the pathophysiology.
Keywords: Endothelial dysfunction / Retinal Arterioles / I/r Injury / Ganglion Cell Loss

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