Key result
Prostaglandin E1 lowers the bradykinin concentration required to inhibit human platelet aggregation by ~89%.
Why the study?
Does prostaglandin E1 at clinically relevant concentrations inhibit platelet aggregation through synergism with endothelial cells?
Population
Human platelets and cultured porcine aortic endothelial (PAE) cells
Comparison
Prostaglandin E1 at clinically relevant… vs PGE1 alone or PAE cell incubation buffer alone
Design
Preclinical
Authors
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May potentiate bradykinin-mediated platelet inhibition; leaves open endothelial synergy and clinical relevance in humans.
Does prostaglandin E1 at clinically relevant concentrations inhibit platelet aggregation through synergism with endothelial cells?
Absolute Event Rate: 10.3% vs 95.4%
PGE1 at clinically relevant concentrations (>=0.1 ng/ml) inhibits platelet aggregation through a synergistic interaction with endothelial cell-derived factors, particularly nitric oxide.
Koga et al. (2002) studied Platelet aggregation. Prostaglandin E1 (PGE1) vs. Bradykinin alone was evaluated on Half-maximum effective concentration of bradykinin to inhibit aggregation. Prostaglandin E1 at clinically relevant concentrations (≥0.1 ng/ml) significantly decreased the half-maximum effective concentration of bradykinin required to inhibit human platelet aggregation.