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Hemodynamic changes and neuronal damage detected by 9.4 T MRI in rats with chronic cerebral ischemia and cognitive impairment

INTRODUCTION: The bilateral common carotid artery occlusion (BCCAO) rat model is an ideal animal model for simulating the pathology of chronic brain hypoperfusion in humans. However, dynamic changes in neuronal activity, cellular edema, and neuronal structural integrity in vivo after BCCAO have rare...

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Autores principales: Sun, Minghua, Wu, Liangmiao, Chen, Guangying, Mo, Xukai, Shi, Changzheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9304847/
https://www.ncbi.nlm.nih.gov/pubmed/35687797
http://dx.doi.org/10.1002/brb3.2642
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author Sun, Minghua
Wu, Liangmiao
Chen, Guangying
Mo, Xukai
Shi, Changzheng
author_facet Sun, Minghua
Wu, Liangmiao
Chen, Guangying
Mo, Xukai
Shi, Changzheng
author_sort Sun, Minghua
collection PubMed
description INTRODUCTION: The bilateral common carotid artery occlusion (BCCAO) rat model is an ideal animal model for simulating the pathology of chronic brain hypoperfusion in humans. However, dynamic changes in neuronal activity, cellular edema, and neuronal structural integrity in vivo after BCCAO have rarely been reported. The purpose of this study is to use a 9.4 T MRI to explore the pathophysiological mechanisms of vascular dementia. MATERIALS AND METHODS: Twelve Sprague–Dawley (SD) rats were randomly divided into two groups: the sham group and the model group (n = 6 for each group). Rats were subjected to MRI using T2*WI, diffusion tensor imaging (DTI), and DWI sequences by MRI at the following six time points: presurgery and 6 h, 3 days, 7 days, 21 days, and 28 days postsurgery. Then, the T2*, fractional anisotropy (FA), and average apparent diffusion coefficient (ADC) values were measured in the bilateral cortices and hippocampi. After MRI scanning, all rats in both groups were subjected to the Y‐maze test, novel object recognition test, and open‐field test to assess their learning, memory, cognition, and locomotor activity. RESULTS: The T2*, FA, and ADC values in the cerebral cortex and hippocampus decreased sharply at 6 h after BCCAO in the model group compared with those of the sham group. By Day 28, the T2* and ADC values gradually increased to close to those in the sham group, but the FA values changed little, and the rats in the model group had worse learning, memory, and cognition and less locomotor activity than the rats in the sham group. CONCLUSIONS: The BCCAO is an ideal rat model for studying the pathophysiological mechanisms of vascular dementia.
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spelling pubmed-93048472022-07-26 Hemodynamic changes and neuronal damage detected by 9.4 T MRI in rats with chronic cerebral ischemia and cognitive impairment Sun, Minghua Wu, Liangmiao Chen, Guangying Mo, Xukai Shi, Changzheng Brain Behav Original Articles INTRODUCTION: The bilateral common carotid artery occlusion (BCCAO) rat model is an ideal animal model for simulating the pathology of chronic brain hypoperfusion in humans. However, dynamic changes in neuronal activity, cellular edema, and neuronal structural integrity in vivo after BCCAO have rarely been reported. The purpose of this study is to use a 9.4 T MRI to explore the pathophysiological mechanisms of vascular dementia. MATERIALS AND METHODS: Twelve Sprague–Dawley (SD) rats were randomly divided into two groups: the sham group and the model group (n = 6 for each group). Rats were subjected to MRI using T2*WI, diffusion tensor imaging (DTI), and DWI sequences by MRI at the following six time points: presurgery and 6 h, 3 days, 7 days, 21 days, and 28 days postsurgery. Then, the T2*, fractional anisotropy (FA), and average apparent diffusion coefficient (ADC) values were measured in the bilateral cortices and hippocampi. After MRI scanning, all rats in both groups were subjected to the Y‐maze test, novel object recognition test, and open‐field test to assess their learning, memory, cognition, and locomotor activity. RESULTS: The T2*, FA, and ADC values in the cerebral cortex and hippocampus decreased sharply at 6 h after BCCAO in the model group compared with those of the sham group. By Day 28, the T2* and ADC values gradually increased to close to those in the sham group, but the FA values changed little, and the rats in the model group had worse learning, memory, and cognition and less locomotor activity than the rats in the sham group. CONCLUSIONS: The BCCAO is an ideal rat model for studying the pathophysiological mechanisms of vascular dementia. John Wiley and Sons Inc. 2022-06-10 /pmc/articles/PMC9304847/ /pubmed/35687797 http://dx.doi.org/10.1002/brb3.2642 Text en © 2022 The Authors. Brain and Behavior published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Sun, Minghua
Wu, Liangmiao
Chen, Guangying
Mo, Xukai
Shi, Changzheng
Hemodynamic changes and neuronal damage detected by 9.4 T MRI in rats with chronic cerebral ischemia and cognitive impairment
title Hemodynamic changes and neuronal damage detected by 9.4 T MRI in rats with chronic cerebral ischemia and cognitive impairment
title_full Hemodynamic changes and neuronal damage detected by 9.4 T MRI in rats with chronic cerebral ischemia and cognitive impairment
title_fullStr Hemodynamic changes and neuronal damage detected by 9.4 T MRI in rats with chronic cerebral ischemia and cognitive impairment
title_full_unstemmed Hemodynamic changes and neuronal damage detected by 9.4 T MRI in rats with chronic cerebral ischemia and cognitive impairment
title_short Hemodynamic changes and neuronal damage detected by 9.4 T MRI in rats with chronic cerebral ischemia and cognitive impairment
title_sort hemodynamic changes and neuronal damage detected by 9.4 t mri in rats with chronic cerebral ischemia and cognitive impairment
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9304847/
https://www.ncbi.nlm.nih.gov/pubmed/35687797
http://dx.doi.org/10.1002/brb3.2642
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