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Frank W Blixt, Sara Johansson, Kristian Agmund Haanes, Karin Warfvinge, Lars Edvinsson; Global Cerebral Ischemia and its Effects on the Retina and Ciliary Artery of the Eye. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):27.
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© ARVO (1962-2015); The Authors (2016-present)
Retinal ischemic diseases account for the majority of retinal blindness in our community. Surprisingly little research has been directed towards the shared factor in all ischemic diseases - the blood vessel wall. Previously, upregulation of the contractile Endotheline-1 (ET-1) and 5-Hydroxytryptamine (5-HT) receptors has been demonstrated in cerebral arteries 48 hours after global cerebral ischemia. The aim of the present study was to investigate if similar phenotypic switching occurs in the retinal vascular bed following global cerebral ischemia.
Rats were subjected to global cerebral ischemia for 15 minutes by two vessel carotid artery occlusion and hypovolemia, or to control operation (sham-operated). The rats were sacrificed at 24h, 48h, 72h, or 7 days, and the eyes were carefully removed. The ciliary arteries of the eye were dissected and mounted on a myograph for functional studies. The eyes were formalin fixed and processed for immunohistochemistry and evaluated for GFAP and Vimentin expression.
Preliminary results showed increased constriction to ET-1, but not to 5-CT, in ciliary arteries of the eye after global cerebral ischemia compared to sham-operation. The monophasic nature of the ET-1 concentration response curve corresponds to ETA receptor-mediated vasoconstriction. In addition, significantly increased Emax was found after the vessels 2 days after ischemia. No significant changes were observed between ischemic and sham operated rats using immunohistochemistry and antibodies against ET-1 and 5-HT receptors. GFAP and Vimentin expression in the retina at 48h was low, while both 72h and 7 day showed strong upregulation of both GFAP and Vimentin.
In conclusion, myograph data suggest an upregulation of ETA receptor 48h after ischemia. The increase in contractility might exacerbate retinal damage after ischemia as seen by the increase of GFAP and Vimentin 72h post ischemia. No difference in immunohistochemistry was observed 24 or 48 hours between sham operated and ischemic animals. This suggests that a decreased blood flow in the retinal artery might play a role in ischemic damage. We also suggest that vasculature supplying the retina with blood may follow the same patterns of cerebral vasculature and therefore may be a key feature to treatment of retinal ischemic conditions.
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