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Inflammatory mediators such as cytokines produced by white blood cells (WBCs) at the site of implantation are important for the biocompatibility of vascular grafts. The aim of the present study was to demonstrate the tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) release from WBCs incubated with expanded polytetrafluoroethylene (ePTFE) or woven Dacron grafts. In a second series the effects of pentoxifylline (PTX) and iloprost (ILO), both known to inhibit white blood cell function, on this release were determined. Woven Dacron grafts induced significantly higher release of both TNF-alpha and IL-6 compared to ePTFE. TNF-alpha was detectable first after 2 h, whereas IL-6 was seen after 4 h. Maximum values were reached at 6 and 12 h, respectively. The addition of an endotoxin gave more pronounced patterns of cytokine release not influenced by time. Preincubation with both PTX and ILO at final concentrations of 100 and 10 micrograms/mL, respectively, reduced significantly the TNF-alpha release without differences between the two graft materials, whereas the effect on the IL-6 release varied and was graft material-dependent. In conclusion, graft material-dependent induction of TNF-alpha and IL-6 from WBCs was demonstrated. PTX and ILO influenced the cytokine release. It might be suggested that graft material-induced cytokine production could contribute to intimal hyperplasia in vivo. The present findings encourage further studies regarding graft material-induced WBC alterations and the role of pharmacologic agents influencing this function.

The expression of surface adhesion molecules on granulocytes, monocytes (CD11a, CD11b, CD11c, CD18, L-selectin), and platelets (P-selectin, gpIIb-IIIa) was determined after incubation with different graft surfaces [expanded polytetrafluoroethylene (ePTFE) or woven Dacron]. Woven Dacron grafts upregulated the CD11b and CD11c surface antigens on both granulocytes and monocytes. Both graft materials demonstrated increased expression of CD11a and CD18 adhesion molecules on white blood cells at 30 min, followed by a downregulation. Maximum L-selectin expression was seen at 120 min on granulocytes and at 90 min on monocytes without differences between the graft materials. A rapid downregulation of gpIIb-IIIa complexes on platelets was noticed, while no expression of platelet P-selectin molecules was observed. In conclusion, both graft materials induced alteration of the white blood cell adhesion molecule expression, but the intensity and time course were dependent on the cell type and the graft material, suggesting that different mechanisms might be implicated. The expression of platelet surface antigens was less clearly influenced. The clinical significance of an enhanced cell surface antigen receptor expression caused by woven Dacron (CD11b, CD11c) has to be further studied. However, determination of adhesion molecule expression might offer possibilities to predict biocompatibility.