Ex vivo Pulsatile Perfusion of Human Saphenous Veins Induces Intimal Hyperplasia and Increased Levels of the Plasminogen Activator Inhibitor 1.

Détails

ID Serval
serval:BIB_B5181A246808
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Ex vivo Pulsatile Perfusion of Human Saphenous Veins Induces Intimal Hyperplasia and Increased Levels of the Plasminogen Activator Inhibitor 1.
Périodique
European Surgical Research
Auteur(s)
Saucy F., Probst H., Alonso F., Bérard X., Déglise S., Dunoyer-Geindre S., Mazzolai L., Kruithof E., Haefliger J.A., Corpataux J.M.
ISSN
1421-9921[electronic], 0014-312X[linking]
Statut éditorial
Publié
Date de publication
2010
Volume
45
Numéro
1
Pages
50-59
Langue
anglais
Résumé
Vessel wall trauma induces vascular remodeling processes including the development of intimal hyperplasia (IH). To assess the development of IH in human veins, we have used an ex vivo vein support system (EVVSS) allowing the perfusion of freshly isolated segments of saphenous veins in the presence of a pulsatile flow which reproduced arterial conditions regarding shear stress, flow rate and pressure during a period of 7 and 14 days. Compared to the corresponding freshly harvested human veins, histomorphometric analysis showed a significant increase in the intimal thickness which was already maximal after 7 days of perfusion. Expression of the endothelial marker CD31 demonstrated the presence of endothelium up to 14 days of perfusion. In our EVVSS model, the activity as well as the mRNA and protein expression levels of plasminogen activator inhibitor 1, the inhibitor of urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA), were increased after 7 days of perfusion, whereas the expression levels of tPA and uPA were not altered. No major change was observed between 7 and 14 days of perfusion. These data show that our newly developed EVVSS is a valuable setting to study ex vivo remodeling of human veins submitted to a pulsatile flow.
Mots-clé
Ex vivo perfusion, Human saphenous vein, Intimal hyperplasia, Fibrinolytic factors, Plasminogen activator inhibitor 1, Urokinase-type plasminogen activator, Tissue-type plasminogen activator, neointima formation, graft failure, shear-stress, model, system, type-1, mice, hypertension, restenosis, responses
Pubmed
Web of science
Création de la notice
22/09/2010 16:11
Dernière modification de la notice
20/08/2019 16:23
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