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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
Authors
Sim J.Jo A.Kang B.-M.Lee S.Bang O.Y.Heo C.Jhon G.-J.Lee Y.Suh M.
Ewha Authors
이영미
SCOPUS Author ID
이영미scopus
Issue Date
2016
Journal Title
Experimental Neurobiology
ISSN
1226-2560JCR Link
Citation
Experimental Neurobiology vol. 25, no. 3, pp. 130 - 138
Keywords
Arterial reactivityHemodynamicsMCAO modelOptical intrinsic signal imagingStroke
Publisher
Korean Society for Neurodegenerative Disease
Indexed
SCOPUS; KCI scopus
Document Type
Article
Abstract
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 realtime 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. © Experimental Neurobiology 2016.
DOI
10.5607/en.2016.25.3.130
Appears in Collections:
자연과학대학 > 화학·나노과학전공 > Journal papers
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