Abstract
AbstractThe effect of pure synthetic PAF (1-O-alkyl-2-acetyl-snglycero-3-phosphorylcholine) was studied in human platelets. PAF (0.2–2.0 µg/ml) produced a dose-dependent aggregation in human platelet-rich plasma (PRP) or platelet suspension obtained by gel-filtration (GFP). In addition, PAF (0.8 µg/ml) induced secretion of 14C-serotonin (45% ± 10%; mean ± SD, n = 9) and platelet factor 4 (PF4) (12.89 ± 3.81 µg/109 platelets; n = 9) in PRP. Similar results were obtained in GFP. Aggregation and release of 14C-serotonin and PF4 were inhibited by the metabolic inhibitors 2-deoxyglucose (16.7 mM) and antimycin-A (8.3 µg/ml), by the membrane-active drugs mepacrine (10 µM) and chlorpromazine (0.025 mM), by PGI2 (5.34 µM), which elevates intracellular c-AMP, by indomethacin (10 µM) or aspirin (100 µM). The ADP scavengers, creatine phosphate and creatine Phosphokinase (CP/CPK), inhibited the second wave of aggregation but not secretion. These data suggest that the major effect of PAF on human platelets is mediated through the cyclo-oxygenase pathway and not through a third pathway.
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