Rapamycin enhances platelet aggregation induced by adenosine diphosphate in vitro.
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.
Wu
Qi
Q
Department of Cardiology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Huang
Kai-Sen
KS
Chen
Mao
M
Huang
De-Jia
DJ
D000244:Adenosine Diphosphate / Q000494:pharmacology*; D000818:Animals; D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects* / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D054855:Drug-Eluting Stents; D010974:Platelet Aggregation / Q000187:drug effects*; D011817:Rabbits; D020123:Sirolimus / Q000494:pharmacology*
D000244:Adenosine Diphosphate; D001241:Aspirin; D020123:Sirolimus