Key result
Aspirin or indomethacin inhibits platelet aggregation on cultured endothelial cells but fails to prevent adhesion.
Aspirin and indomethacin inhibit platelet aggregation but not adhesion in a novel in vitro model of platelet thrombi on cultured endothelial cells.
Supports distinct effects on aggregation versus adhesion in endothelial models; leaves open translation to clinical practice.
Platelet adhesion and aggregation were induced on cultured endothelial cells using the fluorescent dye/light method. A cone-and-plate apparatus was newly developed to observe interactions between platelets and cultured endothelial cells under a shear flow condition. The platelet deposition grew on the light-irradiated area of the cells. Degree of endothelial cell injury induced by the dye/light reaction seemed to depend on the dye concentration. Application of either aspirin or indomethacin significantly inhibited the growth of platelet aggregation, but was not effective for the platelet adhesion to endothelial cells. The platelet thrombi were formed on endothelial cells without their denudation. It was found by transmission electron microscopy that platelets directly adhered to endothelial cells which were not seriously damaged. This thrombus model is expected to be applicable to some physiological and pharmacological studies investigating platelet-endothelial cell interaction and mechanism of platelet thrombus formation in blood vessels.
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Sato et al. (1992) studied Platelet thrombus formation. Aspirin or indomethacin was evaluated on Platelet adhesion and aggregation. Aspirin or indomethacin significantly inhibited the growth of platelet aggregation on cultured endothelial cells induced by the dye/light method, but did not prevent platelet adhesion.
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