Inducible platelet adherence to human umbilical vein endothelium by anticardiolipin antibody-positive sera

OBJECTIVE: Our purpose was to determine whether anticardiolipin antibody-positive sera alter platelet adherence to vascular endothelium by a platelet activating factor-dependent mechanism. STUDY DESIGN: Anticardiolipin antibody-positive sera were used in an in vitro platelet-endothelial adherence as...

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Veröffentlicht in:American journal of obstetrics and gynecology 1995-09, Vol.173 (3), p.702-707
Hauptverfasser: Silver, Richard K., Mullen, Tiffany A., Caplan, Michael S., O'Connell, Patti D., Ragin, Ann
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Sprache:eng
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Zusammenfassung:OBJECTIVE: Our purpose was to determine whether anticardiolipin antibody-positive sera alter platelet adherence to vascular endothelium by a platelet activating factor-dependent mechanism. STUDY DESIGN: Anticardiolipin antibody-positive sera were used in an in vitro platelet-endothelial adherence assay. Confluent endothelial monolayers were randomly assigned for exposure to a 20% concentration of experimental and control sera. Platelets were radiolabeled with chromium 51, and adherence was assessed by quantification of endothelium-associated gamma emission. RESULTS: Inducible platelet adherence was observed by endothelial cell preincubation with sera from anticardiolipin antibody-positive donors compared with anticardiolipin antibody-negative control experiments ( n = 12, platelet adherence 6.4% ± 1.3% vs 4.5% ± 1.1%, respectively; p = 0.02). Compared with endothelial cell incubations alone, coincubation of platelets with anticardiolipin antibody-positive sera consistently augmented primary adherence ( n = 6, p = 0.042). Furthermore, platelet adherence induced by antibody-positive sera was consistently attenuated by specific platelet-activating factor antagonists in a dose-dependent fashion ( p < 0.001) and was restored by exogenously administered platelet-activating factor. CONCLUSIONS: Anticardiolipin antibody-induced platelet adherence may constitute an important prerequisite for vascular thrombosis in antibody-positive patients. The findings from this in vitro model suggest direct involvement of platelet-activating factor in this process.
ISSN:0002-9378
1097-6868
DOI:10.1016/0002-9378(95)90326-7