Inhibition Of Aspirin And Clopidogrel On Platelet Activion Of Rabbit Induced By Unfractionated Heparin

Objective: To evaluate the inhibition of aspirin, clopidogrel and their combination on platelet activation of rabbit induced by unfractionated heparin (UFH) .Methods: 16 rabbits were randomly divided into two groups respectively. The aspirin group was receiving the intragastric administration of aspirin (12mg/Kg.d) during 1~7 days, and the combination with clopidogrel (4mg/Kg.d) in the next 7 days. So did the clopidogrel group. The total intervention lasted 14 days.Each rabbit received UFH at the same time of the 1st, 7th 14th day, and blood was sampled before and after the intravenous injection of UFH . The platelet aggregation was performed using whole blood aggregometers (chrono-log); the plasma concentration of vWF and the level of CD62p were measured in duplicate with enzyme linked immunosorbent assay (ELISA) technique.Result: 1.Effects of heparin on activation of platelet:ADP- induced platelet aggregation 30 minute after intravenous injection of UFH was significantly higher than that before the injection(P<0.05).But neither AA nor Epinephrin-induced platelet aggregation was(P>0.05).The levels of plasma CD62p and vWF before and after intravenous injection of UFH were not significantly different(P>0.05).2.Effects of aspirin on heparin-induced platelet aggregation: After application of aspirin for 7days,ADP,AA,Epi-induced platelet aggregation and levels of plasma CD62p,vWF before and after intravenous injection of UFH were not significantly different (P>0.05).After the intervention of aspirin, platelet ag- gregation before and after intravenous injection of UFH were not significantly different from those under baseline(P>0.05).3.Effects of clopidogrel on heparin-induced platelet ag- gregation: After application of clopidogrel for 7days,ADP,AA,Epi- induced platelet aggregation and levels of plasma CD62p,vWF before and after intravenous injection of UFH were not significantly different(P>0.05). After the intervention of clopidogrel, platelet aggregation before intravenous injection of UFH was not significantly different from that at baseline, but ADP- induced platelet aggregation after intravenous injection of UFH was significantly lower than that at baseline(P<0.05). But neither AA nor Epinephrin-induced platelet aggregation was different from that at baseline(P>0.05).4.Effects of combination of aspirin and clopidogrel on heparin-induced platelet aggregation:After intervention of clopi- dogrel and aspirin for 7 days,the levels of plasma vWF 30 mi- nutes after intravenous injection of UFH was significantly lower than that before the injection(P<0.05).After intervention of aspi -rin and clopidogrel for 7 days,ADP,AA,Epi-induced platelet aggregation and the levels of plasma CD62p before and after in- travenous injection of UFH were not significantly different(P>0.05).But under the combination,ADP-induced platelet aggregation both before and after intravenous injection of UFH were significantlylower than that at baseline and that after the intervention of clopidogrel for 7 days(P<0.05).Conclusion: Heparins potentiate ADP-induced platelet activation. This potentiation is attenuated by clopidogrel or its combination with aspirin. ADP receptor antagonists may have potential therapeutic benefits in counteracting the pro- thrombotic effects of heparins.