Document Detail


A model of cerebrovascular injury in rats.
MedLine Citation:
PMID:  18786566     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although the pathophysiology of post-angioplasty restenosis has been extensively studied in extracranial arteries using transluminal vascular injury model in rodents, it is still not well known in the intracranial arteries, which have quite different structures from extracranial arteries. Here, we examined whether 1-min placement of modified intraluminal suture could induce an injury in the internal carotid artery (ICA) in rats and observed temporal profile of histological change after the injury. HE staining showed that the injured intracranial ICA was dilated, while the media was markedly thinned at 1 day after injury. The internal elastic lamina was not observed, and the media contained few cells. At 1 week after injury, a thin layer of neointimal hyperplasia was observed on the luminal side of the internal elastic lamina. Neointimal hyperplasia developed until at least 4 weeks after injury. Morphometric analysis demonstrated that the healing process of the injury was related to arterial remodeling. Immunohistochemical staining for alpha-smooth muscle actin and electron microscopic analysis showed that the neointima was composed of smooth muscle cells. Re-endothelialization was observed from 1 to 4 weeks after injury by immunohistochemical staining for von Willebrand's factor and electron microscopic analysis. Vascular endothelial growth factor was expressed in neointima on days 7 and 14. Interestingly, superoxide anion was not increased in injured arteries on day 3, when the infiltration of macrophages was intensive, but increased on day 7, when infiltrating macrophages almost disappeared. These findings might shed new light on pathophysiology of post-angioplasty restenosis in intracranial arteries.
Authors:
Kouji Wakayama; Munehisa Shimamura; Masataka Sata; Nobutaka Koibuchi; Naoyuki Sato; Toshio Ogihara; Ryuichi Morishita
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-08-22
Journal Detail:
Title:  Journal of neuroscience methods     Volume:  175     ISSN:  0165-0270     ISO Abbreviation:  J. Neurosci. Methods     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-10-22     Completed Date:  2009-04-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905558     Medline TA:  J Neurosci Methods     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  187-95     Citation Subset:  IM    
Affiliation:
Department of Advanced Clinical Science and Therapeutics, Graduate School of Medicine, University of Tokyo, Japan.
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MeSH Terms
Descriptor/Qualifier:
Actins / metabolism
Animals
Antigens, CD / metabolism
Antigens, Differentiation, Myelomonocytic / metabolism
Arteries / metabolism,  pathology
Basement Membrane / metabolism,  pathology,  ultrastructure
Cerebrovascular Disorders* / metabolism,  pathology,  physiopathology
Disease Models, Animal*
Endothelium, Vascular / metabolism,  pathology,  ultrastructure
Gene Expression Regulation / physiology
Male
Microscopy, Electron, Transmission
Rats
Rats, Wistar
Time Factors
Vascular Endothelial Growth Factor A / metabolism
von Willebrand Factor / immunology,  metabolism
Chemical
Reg. No./Substance:
0/Actins; 0/Antigens, CD; 0/Antigens, Differentiation, Myelomonocytic; 0/CD68 antigen, human; 0/Vascular Endothelial Growth Factor A; 0/Von Willebrand antigen; 0/von Willebrand Factor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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