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Cerebral Hemodynamics and Vascular Reactivity in Mild and Severe Ischemic Rodent Middle Cerebral Artery Occlusion Stroke Models
Ischemia can cause decreased cerebral neurovascular coupling, leading to a failure in the autoregulation of cerebral blood flow. This study aims to investigate the effect of varying degrees of ischemia on cerebral hemodynamic reactivity using in vivo real-time optical imaging. We utilized direct cor...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Korean Society for Brain and Neural Science
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4923357/ https://www.ncbi.nlm.nih.gov/pubmed/27358581 http://dx.doi.org/10.5607/en.2016.25.3.130 |
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author | Sim, Jeongeun Jo, Areum Kang, Bok-Man Lee, Sohee Bang, Oh Young Heo, Chaejeong Jhon, Gil-Ja Lee, Youngmi Suh, Minah |
author_facet | Sim, Jeongeun Jo, Areum Kang, Bok-Man Lee, Sohee Bang, Oh Young Heo, Chaejeong Jhon, Gil-Ja Lee, Youngmi Suh, Minah |
author_sort | Sim, Jeongeun |
collection | PubMed |
description | Ischemia can cause decreased cerebral neurovascular coupling, leading to a failure in the autoregulation of cerebral blood flow. This study aims to investigate the effect of varying degrees of ischemia on cerebral hemodynamic reactivity using in vivo real-time optical imaging. We utilized direct cortical stimulation to elicit hyper-excitable neuronal activation, which leads to induced hemodynamic changes in both the normal and middle cerebral artery occlusion (MCAO) ischemic stroke groups. Hemodynamic measurements from optical imaging accurately predict the severity of occlusion in mild and severe MCAO animals. There is neither an increase in cerebral blood volume nor in vessel reactivity in the ipsilateral hemisphere (I.H) of animals with severe MCAO. The pial artery in the contralateral hemisphere (C.H) of the severe MCAO group reacted more slowly than both hemispheres in the normal and mild MCAO groups. In addition, the arterial reactivity of the I.H in the mild MCAO animals was faster than the normal animals. Furthermore, artery reactivity is tightly correlated with histological and behavioral results in the MCAO ischemic group. Thus, in vivo optical imaging may offer a simple and useful tool to assess the degree of ischemia and to understand how cerebral hemodynamics and vascular reactivity are affected by ischemia. |
format | Online Article Text |
id | pubmed-4923357 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | The Korean Society for Brain and Neural Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-49233572016-06-29 Cerebral Hemodynamics and Vascular Reactivity in Mild and Severe Ischemic Rodent Middle Cerebral Artery Occlusion Stroke Models Sim, Jeongeun Jo, Areum Kang, Bok-Man Lee, Sohee Bang, Oh Young Heo, Chaejeong Jhon, Gil-Ja Lee, Youngmi Suh, Minah Exp Neurobiol Original Article Ischemia can cause decreased cerebral neurovascular coupling, leading to a failure in the autoregulation of cerebral blood flow. This study aims to investigate the effect of varying degrees of ischemia on cerebral hemodynamic reactivity using in vivo real-time optical imaging. We utilized direct cortical stimulation to elicit hyper-excitable neuronal activation, which leads to induced hemodynamic changes in both the normal and middle cerebral artery occlusion (MCAO) ischemic stroke groups. Hemodynamic measurements from optical imaging accurately predict the severity of occlusion in mild and severe MCAO animals. There is neither an increase in cerebral blood volume nor in vessel reactivity in the ipsilateral hemisphere (I.H) of animals with severe MCAO. The pial artery in the contralateral hemisphere (C.H) of the severe MCAO group reacted more slowly than both hemispheres in the normal and mild MCAO groups. In addition, the arterial reactivity of the I.H in the mild MCAO animals was faster than the normal animals. Furthermore, artery reactivity is tightly correlated with histological and behavioral results in the MCAO ischemic group. Thus, in vivo optical imaging may offer a simple and useful tool to assess the degree of ischemia and to understand how cerebral hemodynamics and vascular reactivity are affected by ischemia. The Korean Society for Brain and Neural Science 2016-06 2016-06-22 /pmc/articles/PMC4923357/ /pubmed/27358581 http://dx.doi.org/10.5607/en.2016.25.3.130 Text en Copyright © Experimental Neurobiology 2016. http://creativecommons.org/licenses/by-nc/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Sim, Jeongeun Jo, Areum Kang, Bok-Man Lee, Sohee Bang, Oh Young Heo, Chaejeong Jhon, Gil-Ja Lee, Youngmi Suh, Minah Cerebral Hemodynamics and Vascular Reactivity in Mild and Severe Ischemic Rodent Middle Cerebral Artery Occlusion Stroke Models |
title | Cerebral Hemodynamics and Vascular Reactivity in Mild and Severe Ischemic Rodent Middle Cerebral Artery Occlusion Stroke Models |
title_full | Cerebral Hemodynamics and Vascular Reactivity in Mild and Severe Ischemic Rodent Middle Cerebral Artery Occlusion Stroke Models |
title_fullStr | Cerebral Hemodynamics and Vascular Reactivity in Mild and Severe Ischemic Rodent Middle Cerebral Artery Occlusion Stroke Models |
title_full_unstemmed | Cerebral Hemodynamics and Vascular Reactivity in Mild and Severe Ischemic Rodent Middle Cerebral Artery Occlusion Stroke Models |
title_short | Cerebral Hemodynamics and Vascular Reactivity in Mild and Severe Ischemic Rodent Middle Cerebral Artery Occlusion Stroke Models |
title_sort | cerebral hemodynamics and vascular reactivity in mild and severe ischemic rodent middle cerebral artery occlusion stroke models |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4923357/ https://www.ncbi.nlm.nih.gov/pubmed/27358581 http://dx.doi.org/10.5607/en.2016.25.3.130 |
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