REDISTRIBUTION OF VON-WILLEBRAND-FACTOR IN PORCINE CAROTID ARTERIES AFTER BALLOON ANGIOPLASTY

Citation
Jc. Giddings et al., REDISTRIBUTION OF VON-WILLEBRAND-FACTOR IN PORCINE CAROTID ARTERIES AFTER BALLOON ANGIOPLASTY, Arteriosclerosis, thrombosis, and vascular biology, 17(10), 1997, pp. 1872-1878
Citations number
49
Categorie Soggetti
Peripheal Vascular Diseas
ISSN journal
10795642
Volume
17
Issue
10
Year of publication
1997
Pages
1872 - 1878
Database
ISI
SICI code
1079-5642(1997)17:10<1872:ROVIPC>2.0.ZU;2-F
Abstract
von Willebrand factor (VWF) is a well-characterized multimeric glycopr otein present in platelets and plasma and synthesized by vascular endo thelial cells and megakaryocytes. Its role in platelet-vessel wall int eractions has been studied extensively, but its involvement in intrava scular events after balloon angioplasty has not been clarified. VWF an tigen is not present in porcine arterial endothelium (except for the p ulmonary artery) but is readily detected in porcine venous endothelial cells. We have examined the localization of VWF in porcine vessel wal ls during neointima formation after bilateral carotid balloon-angiopla sty. Endothelium was denuded by balloon injury but regenerated by 7 da ys and was fully confluent by 42 days. VWF was detected at the site of injury in localized, adherent platelet aggregates at 10 minutes after angioplasty that were not present at later time points. A well-demarc ated homogeneous layer of VWF was observed on the luminal surface from 30 minutes to day 7, but there was a progressive shift of positive st aining from the lumen to the outer media from days 1 to 7. VWF was als o strongly detected at sites proximal and distal to the balloon injury from 30 minutes to day 7, although endothelial disruption was minimal and the monolayer remained substantially intact at these sites. Regro wing endothelial cells appeared to contain granular VWF from days 12 t o 21, but this was not readily evident at later time points. The resul ts suggest that balloon injury is associated with deposition and media l absorption of plasma or platelet VWF in this porcine model over a ti me period that precedes and overlaps vascular smooth muscle proliferat ion and endothelial recoverage. The findings provide evidence to suppo rt the concept of a wider role for VWF in tissue injury responses.