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Rapamycin enhances platelet aggregation induced by adenosine diphosphatein vitro

Qi Wu, Kaisen Huang, Mao Chen, Dejia Huang

Open publisher page 20 citations

Abstract

Studies have demonstrated the important role of platelets in the formation of stent thrombosis associated with drug-eluting stents, but little is known about the effects of drugs eluted from stents on platelet function. The extent of platelet aggregation in platelet-rich plasma induced by adenosine diphosphate (ADP) was measured at various doses of rapamycin, and the ability of aspirin to inhibit platelet aggregation was determined at the same concentrations of rapamycin. Compared with lower concentrations, rapamycin at higher doses (>10 ng/mL) enhanced platelet aggregation induced by ADP, and the enhancement was significant at 50 ng/mL and 100 ng/mL (P = 0.005 and P = 0.04). The ability of aspirin to inhibit platelet aggregation was reduced at higher concentrations of rapamycin. These data suggest that higher concentrations of rapamycin can enhance platelet aggregation in response to ADP, and reduce the ability of aspirin to inhibit platelet aggregation.

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What this paper is about

Studies have demonstrated the important role of platelets in the formation of stent thrombosis associated with drug-eluting stents, but little is known about the effects of drugs eluted from stents on platelet function. The extent of platelet aggregation in platelet-rich plasma induced by adenosine diphosphate (ADP) was measured at various doses of rapamycin, and the ability of aspirin to inhibit platelet aggregation was determined at the same concentrations of rapamycin. Compared with lower concentrations, rapamycin at higher doses (>10 ng/mL) enhanced platelet aggregation induced by ADP, and the enhancement was significant at 50 ng/mL and 100 ng/mL (P = 0.005 and P = 0.04). The ability of aspirin to inhibit platelet aggregation was reduced at higher concentrations of rapamycin. These data suggest that higher concentrations of rapamycin can enhance platelet aggregation in response to ADP, and reduce the ability of aspirin to inhibit platelet aggregation.

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Available abstract

Studies have demonstrated the important role of platelets in the formation of stent thrombosis associated with drug-eluting stents, but little is known about the effects of drugs eluted from stents on platelet function. The extent of platelet aggregation in platelet-rich plasma induced by adenosine diphosphate (ADP) was measured at various doses of rapamycin, and the ability of aspirin to inhibit platelet aggregation was determined at the same concentrations of rapamycin. Compared with lower concentrations, rapamycin at higher doses (>10 ng/mL) enhanced platelet aggregation induced by ADP, and the enhancement was significant at 50 ng/mL and 100 ng/mL (P = 0.005 and P = 0.04). The ability of aspirin to inhibit platelet aggregation was reduced at higher concentrations of rapamycin. These data suggest that higher concentrations of rapamycin can enhance platelet aggregation in response to ADP, and reduce the ability of aspirin to inhibit platelet aggregation.

Key concepts: Platelet, Adenosine diphosphate, Aspirin, Chemistry, Platelet aggregation, In vitro, Pharmacology, Adenosine

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