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Enhancement of sickle erythrocyte adherence to endothelium by autologous platelets
Author(s) -
Antonucci Richard,
Walker Richard,
Herion John,
Orringer Eugene
Publication year - 1990
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830340110
Subject(s) - platelet , prostacyclin , endothelium , umbilical vein , epinephrine , platelet adhesiveness , thromboxane a2 , aspirin , medicine , endocrinology , chemistry , hemolysis , immunology , pharmacology , platelet aggregation , biochemistry , in vitro
The increased adhesiveness of sickle erythrocytes (SS RBC) to endothelial cells has been confirmed in a static system utilizing fresh umbilical vein endothelium. Adherence of SS RBC to the endothelium was as great in the presence of calcium‐containing buffer as when incubated in plasma. SS RBC suspended in autologous platelet‐rich plasma adhered to a greater extent than when suspended in autologous platelet poor plasma. Prostacyclin, thromboxane B 2 , and an inhibitor of collagen‐ and epinephrine‐induced platelet aggregation (B13.177) did not affect SS RBC adherence to endothelium. Aspirin in concentration of 5 μg/ml slightly decreased SS RBC adherence to endothelium in the presence of platelats may play a significant role in the increased adhesiveness of SS RBC to endothelium. To the extent that increasede SS RBC adhesiveness contributes to the genesis of painful crises and to the extent platelets augment this adhesiveness, agents affecting platelet function may prove useful in preventing painful crises.