INDUCIBLE PLATELET ADHERENCE TO HUMAN UMBILICAL VEIN ENDOTHELIUM BY ANTICARDIOLIPIN ANTIBODY-POSITIVE SERA

Citation
Rk. Silver et al., INDUCIBLE PLATELET ADHERENCE TO HUMAN UMBILICAL VEIN ENDOTHELIUM BY ANTICARDIOLIPIN ANTIBODY-POSITIVE SERA, American journal of obstetrics and gynecology, 173(3), 1995, pp. 702-707
Citations number
25
Categorie Soggetti
Obsetric & Gynecology
ISSN journal
00029378
Volume
173
Issue
3
Year of publication
1995
Part
1
Pages
702 - 707
Database
ISI
SICI code
0002-9378(1995)173:3<702:IPATHU>2.0.ZU;2-8
Abstract
OBJECTIVE: Our purpose was to determine whether anticardiolipin antibo dy-positive sera alter platelet adherence to vascular endothelium by a platelet activating factor-dependent mechanism. STUDY DESIGN: Anticar diolipin antibody-positive sera were used in an in vitro platelet-endo thelial adherence assay. Confluent endothelial monolayers were randoml y assigned for exposure to a 20% concentration of experimental and con trol sera. Platelets were radiolabeled with chromium 51, and adherence was assessed by quantification of endothelium-associated gamma emissi on. RESULTS: Inducible platelet adherence was observed by endothelial cell preincubation with sera from anticardiolipin antibody-positive do nors compared with anticardiolipin antibody-negative control experimen ts (n = 12, platelet adherence 6.4% +/- 1.3% vs 4.5% +/- 1.1%, respect ively; p = 0.02). Compared with endothelial cell incubations alone, co incubation of platelets with anticardiolipin antibody-positive sera co nsistently augmented primary adherence (n = 6, p = 0.042). Furthermore , platelet adherence induced by antibody-positive sera was consistentl y attenuated by specific platelet-activating factor antagonists in a d ose-dependent fashion (p < 0.001) and was restored by exogenously admi nistered platelet-activating factor. CONCLUSIONS: Anticardiolipin anti body-induced platelet adherence may constitute an important prerequisi te for vascular thrombosis in antibody-positive patients. The findings from this in vitro model suggest direct involvement of platelet-activ ating factor in this process.