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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.

Microcalorimetry was used to study in vitro the metabolic response from human platelets and leukocytes when incubated with three different synthetic graft-materials. The graft to be studied primarily was Fluoromer Passivated Dacron (FPD) which was compared with ePTFE and with a knitted Teflon graft. A rapid increase in the metabolic activity of platelets was observed, followed by a steady-state for more than one hour, while the platelet metabolism did not differ among the various graft-materials. Leukocytes incubated with FPD showed a high initial metabolism, with a peak after about 15 minutes. After 60 minutes the metabolic response had reached control values. ePTFE and Teflon grafts differed significantly from FPD, without causing any peak metabolic activity. It may be concluded that FPD and ePTFE grafts, as evaluated in vitro, activate platelets to the same extent, while FPD causes a more extensive leukocyte activation. Whether these findings can be interpreted as differences in thrombogenicity and inflammatory responses has not been proven, but seems probable. This in vitro method should make it possible to further study human responses to synthetic materials a method possibly more reliable than animal experiments.

Purpose: This study was designed to compare deposition of 111In-labeled platelets and neutrophils after balloon angioplasty (PTA) alone and PTA plus Wallstents., Methods: Histological investigation was performed with scanning electron microscopy (SEM). Fifty percent stenoses of both iliac arteries was created by resorbable ligature in 13 pigs. After 30 days, PTA was performed bilaterally with an additional stenting procedure done on one side. Autologous platelets were labeled and reinfused before the interventional procedure in six pigs, and labeled neutrophils were used in seven pigs. The deposition of the labeled cells was recorded in vivo over 270 min using a scintillation camera. The results were correlated with in vitro measurements., Results: Scanning revealed significant increase in platelet and neutrophil deposition at the site of the stent compared with the site where PTA alone was undertaken. In vitro measurements confirmed these differences. SEM demonstrated a fibrin lining on the stent surface and numerous adherent platelets. The adjacent arterial lumen was almost completely covered by fibrinous material. The PTA-alone site demonstrated denudation of endothelial cells and less fibrinous material, as well as platelets and leukocytes., Conclusion: The complex interaction in the response of the vessel wall and flowing blood involves both platelet and neutrophil adhesion. The self-expandable vascular endoprosthesis contributes to increased deposition of platelets and neutrophils as seen in this experimental model of nonatheromatous stenosis.