Cerebral vasculature is often the target of
stroke studies. However, the vasculature supplying the eye might also be affected by
ischemia. The aim of the present study was to investigate if the transient global
cerebral ischemia (GCI) enhances vascular effect of
endothelin-1 (ET-1) and
5-hydroxytryptamine/
serotonin (5-HT) on the ophthalmic artery in rats, leading to delayed
retinal damage. This was preformed using myography on the ophthalmic artery, coupled with immunohistochemistry and electroretinogram (ERG) to assess the ischemic consequences on the retina. Results showed a significant increase of ET-1 mediated vasoconstriction at 48 hours post
ischemia. The retina did not exhibit any morphological changes throughout the study. However, we found an increase of GFAP and
vimentin expression at 72 hours and 7 days after
ischemia, indicating Müller cell mediated
gliosis. ERG revealed significantly decreased function at 72 hours, but recovered almost completely after 7 days. In conclusion, we propose that the increased contractile response via ET-1 receptors in the ophthalmic artery after 48 hours may elicit negative
retinal consequences due to a second ischemic period. This may exacerbate
retinal damage after
ischemia as illustrated by the decreased
retinal function and Müller cell activation. The ophthalmic artery and ET-1 mediated vasoconstriction may be a valid and novel therapeutic target after longer periods of ischemic insults.