Iloprost and tissue-type plasminogen activator differentially affect platelet aggregation in platelet-rich plasma and in whole blood.
Platelet aggregation in platelet-rich plasma (PRP) is more sensitive to agonists and more resistant to antagonists than that in whole blood. In this study, we show that the presence of neutrophils in whole blood accounts at least in part for diminished platelet aggregation in whole blood. The platelet-inhibitory effect of neutrophils relates to the release of nitric oxide and not to elastase or adenosine. Furthermore, two unrelated platelet inhibitors, iloprost and tissue-type plasminogen inhibitor, decrease platelet aggregation to a greater extent in whole blood than in PRP. However, these agents exert cumulative or synergistic inhibitory effects with neutrophils on platelet aggregation in PRP. Thus, the inhibition of platelet aggregation in vivo may relate to the interaction between neutrophils and platelet-inhibitory agents.
Nicolini
F A
FA
Division of Cardiology, University of Florida College of Medicine, Gainesville.
Mehta
J L
JL
D001790:Blood Physiological Phenomena; D002450:Cell Communication / Q000502:physiology; D006801:Humans; D016285:Iloprost / Q000494:pharmacology*; D066298:In Vitro Techniques; D009504:Neutrophils / Q000502:physiology; D010196:Pancreatic Elastase / Q000097:blood; D010949:Plasma / Q000166:cytology* / Q000502:physiology; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D010976:Platelet Count; D010959:Tissue Plasminogen Activator / Q000494:pharmacology*
D010975:Platelet Aggregation Inhibitors; D010196:Pancreatic Elastase; D010959:Tissue Plasminogen Activator; D016285:Iloprost