[High-porosity and normal-porosity prostheses. Differences in growth factor release].

BACKGROUND

The majority of mid- and long-term synthetic vascular graft failures are due to anastomotic neointimal fibrous hyperplasia. The major cause of this phenomenon is the absence of an endothelial lining within prosthetic grafts. We investigated the PDGF-BB and bFGF release by umbilical vein endothelial cell cultured on precoated standard porosity or high porosity expanded polytetrafluoroethylene (ePTFE) vascular grafts.

METHODS

Endothelial cell harvested from umbilical veins were cultured into standard (30 microns internodal distance) or high porosity (60 microns internodal distance) cPTFE disks. ePTFE disks uncoated or precoated with collagen type I, fibronectin and Matrigel were used and endothelial cell cultured into plastic wells coated as ePTFE disks or uncoated plastic wells served as controls. Scanning electron microscopy study assessed endothelial cell coverage. The presence of PDGF-BB and bFGF in serum-free conditioned media from endothelial cells cultured into ePTFE grafts and endothelial cell cultured into wells was determined by the inhibition antibody-binding assay 48 hours after insertion.

RESULTS

Endothelial cell coverage was similar in uncoated and coated ePTFE grafts and no differences were observed between standard or high porosity grafts. The release of PDGF-BB and bFGF was significantly higher either for standard porosity or high porosity ePTFE grafts as compared with endothelial cell cultured into plastic wells (p < 0.05 and p < 0.05, respectively). The release of PDGF-BB and bFGF was independent from the various substrates either for endothelial cell cultured into standard or high porosity ePTFE grafts or plastic wells.

CONCLUSIONS

Our findings pointed out that in ePTFE grafts smooth muscle cellsc proliferated only under endothelial cell at the anastomoses, along seeded synthetic grafts or in areas of transmural ingrowth where smooth muscle cells followed endothelial cell migrating into the graft. This is probably due to an alteration of the interactions between the endothelial cell, the matrices and the synthetic prosthesis.