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A Journal on Angiology
Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
International Angiology 2002 September;21(3):250-5
Induction of angiotensin converting enzyme in neointima after intravascular stent placement
Nishibe T. *, Miyazaki K. *, Kudo F. 1, Flores J. 1, Miyazaki K. 1, Nagato M. 2, Kumada T. 2, Yasuda K. 1
1 Department of Cardiovascular Surgery, Hokkaido University School of Medicine, Sapporo, Japan
2 Daiichi Pharmaceutical Co., Ltd., Tokyo, Japan
Background. To investigate the morphological changes of the arterial wall and the expression of angiotensin converting enzyme (ACE) in the arterial wall after stent placement in a canine model.
Methods. Seventeen mongrel dogs underwent stent placement (Gianturco’s Z stent) in the aorta. Six animals were sacrificed at 4 weeks after stent implantation, and the other 5 animals at 12 weeks. The normal aorta was harvested from 6 dogs. The specimens were stained with hematoxylin-eosin (H&E) as well as by immunohistochemistry (smooth muscle specific α-actin, and ACE). Histomorphometric analysis was performed using the sections stained with H&E and smooth muscle specific α-actin.
Results. The total intimal area was significantly increased at all time points as compared with the control aorta. The α-actin positive intimal area was also significantly increased at all time points as compared with the control aorta. In the control aorta, luminal endothelial cells as well as α-actin positive medial cells occasionally exhibited faint cytoplasmic staining for ACE. In the 4- and 12-week stented aorta, α-actin positive cells in the neointima and media as well as macrophages in the adventitia stained strongly positive for ACE.
Conclusions. ACE was induced in the neointima after stent placement of the canine aorta. Considering its multiple biological actions, ACE may be associated with the pathogenesis of neointimal hyperplasia after stent placement.