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Chronic photoperiod disruption does not increase vulnerability to focal cerebral ischemia in young normotensive rats
Photoperiod disruption, which occurs during shift work, is associated with changes in metabolism or physiology (e.g. hypertension and hyperglycaemia) that have the potential to adversely affect stroke outcome. We sought to investigate if photoperiod disruption affects vulnerability to stroke by dete...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5669340/ https://www.ncbi.nlm.nih.gov/pubmed/27789784 http://dx.doi.org/10.1177/0271678X16671316 |
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author | Ku Mohd Noor, Ku Mastura Wyse, Cathy Roy, Lisa A Biello, Stephany M McCabe, Christopher Dewar, Deborah |
author_facet | Ku Mohd Noor, Ku Mastura Wyse, Cathy Roy, Lisa A Biello, Stephany M McCabe, Christopher Dewar, Deborah |
author_sort | Ku Mohd Noor, Ku Mastura |
collection | PubMed |
description | Photoperiod disruption, which occurs during shift work, is associated with changes in metabolism or physiology (e.g. hypertension and hyperglycaemia) that have the potential to adversely affect stroke outcome. We sought to investigate if photoperiod disruption affects vulnerability to stroke by determining the impact of photoperiod disruption on infarct size following permanent middle cerebral artery occlusion. Adult male Wistar rats (210–290 g) were housed singly under two different light/dark cycle conditions (n = 12 each). Controls were maintained on a standard 12:12 light/dark cycle for nine weeks. For rats exposed to photoperiod disruption, every three days for nine weeks, the lights were switched on 6 h earlier than in the previous photoperiod. T(2)-weighted magnetic resonance imaging was performed at 48 h after middle cerebral artery occlusion. Disruption of photoperiod in young healthy rats for nine weeks did not alter key physiological variables that can impact on ischaemic damage, e.g. blood pressure and blood glucose immediately prior to middle cerebral artery occlusion. There was no effect of photoperiod disruption on infarct size after middle cerebral artery occlusion. We conclude that any potentially adverse effect of photoperiod disruption on stroke outcome may require additional factors such as high fat/high sugar diet or pre-existing co-morbidities. |
format | Online Article Text |
id | pubmed-5669340 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-56693402018-11-01 Chronic photoperiod disruption does not increase vulnerability to focal cerebral ischemia in young normotensive rats Ku Mohd Noor, Ku Mastura Wyse, Cathy Roy, Lisa A Biello, Stephany M McCabe, Christopher Dewar, Deborah J Cereb Blood Flow Metab Original Articles Photoperiod disruption, which occurs during shift work, is associated with changes in metabolism or physiology (e.g. hypertension and hyperglycaemia) that have the potential to adversely affect stroke outcome. We sought to investigate if photoperiod disruption affects vulnerability to stroke by determining the impact of photoperiod disruption on infarct size following permanent middle cerebral artery occlusion. Adult male Wistar rats (210–290 g) were housed singly under two different light/dark cycle conditions (n = 12 each). Controls were maintained on a standard 12:12 light/dark cycle for nine weeks. For rats exposed to photoperiod disruption, every three days for nine weeks, the lights were switched on 6 h earlier than in the previous photoperiod. T(2)-weighted magnetic resonance imaging was performed at 48 h after middle cerebral artery occlusion. Disruption of photoperiod in young healthy rats for nine weeks did not alter key physiological variables that can impact on ischaemic damage, e.g. blood pressure and blood glucose immediately prior to middle cerebral artery occlusion. There was no effect of photoperiod disruption on infarct size after middle cerebral artery occlusion. We conclude that any potentially adverse effect of photoperiod disruption on stroke outcome may require additional factors such as high fat/high sugar diet or pre-existing co-morbidities. SAGE Publications 2016-10-10 2017-11 /pmc/articles/PMC5669340/ /pubmed/27789784 http://dx.doi.org/10.1177/0271678X16671316 Text en © The Author(s) 2016 http://creativecommons.org/licenses/by-nc/3.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Articles Ku Mohd Noor, Ku Mastura Wyse, Cathy Roy, Lisa A Biello, Stephany M McCabe, Christopher Dewar, Deborah Chronic photoperiod disruption does not increase vulnerability to focal cerebral ischemia in young normotensive rats |
title | Chronic photoperiod disruption does not increase vulnerability to focal cerebral ischemia in young normotensive rats |
title_full | Chronic photoperiod disruption does not increase vulnerability to focal cerebral ischemia in young normotensive rats |
title_fullStr | Chronic photoperiod disruption does not increase vulnerability to focal cerebral ischemia in young normotensive rats |
title_full_unstemmed | Chronic photoperiod disruption does not increase vulnerability to focal cerebral ischemia in young normotensive rats |
title_short | Chronic photoperiod disruption does not increase vulnerability to focal cerebral ischemia in young normotensive rats |
title_sort | chronic photoperiod disruption does not increase vulnerability to focal cerebral ischemia in young normotensive rats |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5669340/ https://www.ncbi.nlm.nih.gov/pubmed/27789784 http://dx.doi.org/10.1177/0271678X16671316 |
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