Key result
Aspirin completely suppresses platelet secretion at low PAF-acether concentrations but only partially at high doses.
Why the study?
The effects of cyclo-oxygenase inhibition on PAF-acether-induced human platelet aggregation and secretion are controversial.
Does in vivo administration of acetylsalicylic acid inhibit PAF-acether-induced platelet aggregation and secretion in normal subjects?
Population
12 normal subjects with citrated platelet-rich plasma
Comparison
Before and after in vivo administration of acetylsalicylic acid with or without CaCl2 2 mM exposure
Design
Experimental study on platelet-rich plasma samples
Authors
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ASA fully blocks low-dose PAF secretion but only partially at higher doses; hypothesis-generating for cyclo-oxygenase role, needs confirmation.
Does in vivo administration of acetylsalicylic acid inhibit PAF-acether-induced platelet aggregation and secretion in normal subjects?
Low concentrations of PAF-acether stimulate human platelet secretion via the cyclo-oxygenase pathway, whereas higher concentrations trigger additional mechanisms independent of cyclo-oxygenase.
Cattaneo et al. (1985) studied Normal subjects (n=12). Acetylsalicylic acid (ASA) vs. Before ASA administration (baseline) was evaluated on Platelet aggregation and secretion induced by PAF-acether. In vivo administration of acetylsalicylic acid completely inhibited platelet secretion induced by low concentrations of PAF-acether, but only partially inhibited it at high concentrations.
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