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[Effect of flurbiprofen on platelet functions. Study of its interference with the synthesis of platelet thromboxane and production of prostacyclin by the rabbit aorta].

S Lévy-Toledano, Jacques Maclouf, J Caen, L. Bara, C Lecrubier, M Samama

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Abstract

The effect of flurbiprofen has been studied on the platelet aggregation of a human platelet rich plasma in the presence of 3 different inducers: ADP, collagen and arachidonic acid. Flurbiprofen is a potent inhibitor of platelet aggregation as compared to aspirin (160 to 2200 more potent). This inhibition was also found using isolated platelets stimulated by arachidonic acid where the suppression of the thromboxane synthesis was accompanied by the inhibition of 14C-serotonin release as well as of aggregation. The administration of flurbiprofen to rabbits, 1 and 3 mg/kg during 3 days was followed by an inhibition of the collagen-induced platelet reactivity. The aortic prostacyclin synthesis as studied by its biological activity was also inhibited at 3 mg/kg (p less than 0,01) but less significantly at 1 mg/kg. The more potent action of flurbiprofen compared to that of aspirin as well as its rapid reversibility would allow the use of this drug for the inhibition of some of the platelet functions.

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The effect of flurbiprofen has been studied on the platelet aggregation of a human platelet rich plasma in the presence of 3 different inducers: ADP, collagen and arachidonic acid. Flurbiprofen is a potent inhibitor of platelet aggregation as compared to aspirin (160 to 2200 more potent). This inhibition was also found using isolated platelets stimulated by arachidonic acid where the suppression of the thromboxane synthesis was accompanied by the inhibition of 14C-serotonin release as well as of aggregation. The administration of flurbiprofen to rabbits, 1 and 3 mg/kg during 3 days was followed by an inhibition of the collagen-induced platelet reactivity. The aortic prostacyclin synthesis as studied by its biological activity was also inhibited at 3 mg/kg (p less than 0,01) but less significantly at 1 mg/kg. The more potent action of flurbiprofen compared to that of aspirin as well as its rapid reversibility would allow the use of this drug for the inhibition of some of the platelet functions.

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Available abstract

The effect of flurbiprofen has been studied on the platelet aggregation of a human platelet rich plasma in the presence of 3 different inducers: ADP, collagen and arachidonic acid. Flurbiprofen is a potent inhibitor of platelet aggregation as compared to aspirin (160 to 2200 more potent). This inhibition was also found using isolated platelets stimulated by arachidonic acid where the suppression of the thromboxane synthesis was accompanied by the inhibition of 14C-serotonin release as well as of aggregation. The administration of flurbiprofen to rabbits, 1 and 3 mg/kg during 3 days was followed by an inhibition of the collagen-induced platelet reactivity. The aortic prostacyclin synthesis as studied by its biological activity was also inhibited at 3 mg/kg (p less than 0,01) but less significantly at 1 mg/kg. The more potent action of flurbiprofen compared to that of aspirin as well as its rapid reversibility would allow the use of this drug for the inhibition of some of the platelet functions.

Key concepts: Flurbiprofen, Prostacyclin, Platelet, Chemistry, Arachidonic acid, Thromboxane, Aspirin, Pharmacology

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[Effect of flurbiprofen on platelet functions. Study of its interference with the synthesis of platelet thromboxane and production of prostacyclin by the rabbit aorta]. — Research Paper | ScholarLens