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Enhanced endothelin-1 mediated vasoconstriction of the ophthalmic artery may exacerbate retinal damage after transient global cerebral ischemia in rat

Blixt, Frank W. LU ; Johansson, Sara Ellinor LU ; Johnson, Leif LU ; Haanes, Kristian Agmund; Warfvinge, Karin LU and Edvinsson, Lars LU (2016) In PLoS One 11(6).
Abstract

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.... (More)

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.

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author
organization
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type
Contribution to journal
publication status
published
subject
in
PLoS One
volume
11
issue
6
publisher
Public Library of Science
external identifiers
  • Scopus:84976601100
ISSN
1932-6203
DOI
10.1371/journal.pone.0157669
language
English
LU publication?
yes
id
6c2b6bb6-d4c2-4f45-aea3-17ae529e2de2
date added to LUP
2016-07-20 13:42:04
date last changed
2016-11-03 14:33:39
@misc{6c2b6bb6-d4c2-4f45-aea3-17ae529e2de2,
  abstract     = {<p>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.</p>},
  author       = {Blixt, Frank W. and Johansson, Sara Ellinor and Johnson, Leif and Haanes, Kristian Agmund and Warfvinge, Karin and Edvinsson, Lars},
  issn         = {1932-6203},
  language     = {eng},
  month        = {06},
  number       = {6},
  publisher    = {ARRAY(0xbe31a68)},
  series       = {PLoS One},
  title        = {Enhanced endothelin-1 mediated vasoconstriction of the ophthalmic artery may exacerbate retinal damage after transient global cerebral ischemia in rat},
  url          = {http://dx.doi.org/10.1371/journal.pone.0157669},
  volume       = {11},
  year         = {2016},
}