Growth factors and experimental arterial grafts

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The production of growth factors from several experimental arterial conduits was determined.


We implanted 105 experimental arterial grafts that were 1 cm long in the abdominal aorta of Lewis rats (average weight, 250 g). Five different types of grafts were analyzed: arterial isografts, vein grafts, arterial allografts, and polytetrafluoroethylene (PTFE) grafts with normal or decreased compliance. Animals were killed humanely 4 weeks after surgery and the production of platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF), transforming growth factor-β, tumor necrosis factor-α, and interleukin-1 was analyzed.


Myointimal hyperplasia (MH) was evident in vein grafts, arterial allografts, and PTFE grafts, but not in arterial isografts. Growth factor production was increased for grafts prone to develop MH like vein, PTFE grafts, and arterial allografts. PDGF and bFGF were increased significantly for PTFE and vein grafts, but not for arterial allografts. The importance of bFGF and PGDF was confirmed by the capability of antibody to PDGF and to bFGF to reduce the mitogenic activity of smooth muscle cells, in vivo and in vitro, for PTFE and vein grafts, but not for arterial allografts, in which a predominant role was played by interleukin-1 and tumor necrosis factor-α.


Agents able to neutralize this increased production of growth factors, either directly or by competition with their receptors, can prevent MH formation.

Clinical Relevance:

Arterial grafts release growth factors, which can lead to myointimal hyperplasia formation and atherosclerosis progression in the arterial tree. Both phenomena can cause graft occlusion. Inhibition of growth factor release by arterial grafts can improve their clinical effectiveness.

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