THE DEVELOPMENT OF AN IN-VITRO FLOW MODEL OF HUMAN SAPHENOUS-VEIN GRAFT INTIMAL HYPERPLASIA

Citation
Ke. Porter et al., THE DEVELOPMENT OF AN IN-VITRO FLOW MODEL OF HUMAN SAPHENOUS-VEIN GRAFT INTIMAL HYPERPLASIA, Cardiovascular Research, 31(4), 1996, pp. 607-614
Citations number
44
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00086363
Volume
31
Issue
4
Year of publication
1996
Pages
607 - 614
Database
ISI
SICI code
0008-6363(1996)31:4<607:TDOAIF>2.0.ZU;2-S
Abstract
Objective: Although the role of blood flow has been investigated in an imal models of intimal hyperplasia, there have been no detailed studie s in intact human vein owing to the difficulties in designing a suitab le laboratory model. The aim of this study was to develop a flow model of human vein graft intimal hyperplasia. Methods: Organ cultures of h uman saphenous vein were exposed to laminar flow by culturing in a clo sed circulatory system under predetermined conditions of venous and ar terial shear stress for 14 days. Following fixation and processing, pa raffin sections were immunostained and neointimal thicknesses measured . Results: It was found that arterial flow completely inhibited neoint ima formation, but venous flow only partly suppressed the response whe n compared with vein cultured under static conditions. These results a re in agreement with previous in vivo studies in a primate graft model , where increased shear stress inhibited intimal proliferation. Conclu sion: The endothelial cell is believed to be the key mediator of haemo dynamic effects which influence smooth muscle cell proliferation, and the flow rig developed in this study offers the potential to study int er-cellular interactions within the intact vessel. Furthermore, this m ethod provides the facility to study the effects of different flow con ditions on segments of vein from the same patient. This model has scop e for further development and sophistication which may ultimately lead to increasing our understanding of the aetiology of vein graft stenos es, and hence formulation of preventative strategies.