A model of cerebrovascular injury in rats.
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.
Wakayama
Kouji
K
Department of Advanced Clinical Science and Therapeutics, Graduate School of Medicine, University of Tokyo, Japan.
Shimamura
Munehisa
M
Sata
Masataka
M
Koibuchi
Nobutaka
N
Sato
Naoyuki
N
Ogihara
Toshio
T
Morishita
Ryuichi
R
D000199:Actins / Q000378:metabolism; D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001158:Arteries / Q000378:metabolism / Q000473:pathology; D001485:Basement Membrane / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D002561:Cerebrovascular Disorders / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D005786:Gene Expression Regulation / Q000502:physiology; D008297:Male; D046529:Microscopy, Electron, Transmission; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D014841:von Willebrand Factor / Q000276:immunology / Q000378:metabolism; D000097382:CD68 Molecule
D000199:Actins; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D042461:Vascular Endothelial Growth Factor A; D014841:von Willebrand Factor; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C029417:Von Willebrand antigen