Key result
Infusion of the GPIIb/IIIa-inhibitor MK383 inhibited thrombin generation in platelet rich plasma to a similar extent as 0.2 U/ml of heparin.
Why the study?
Does the GPIIb/IIIa-inhibitor MK383 inhibit thrombin generation in platelet rich plasma from patients?
Does the GPIIb/IIIa-inhibitor MK383 inhibit thrombin generation in platelet rich plasma from patients?
The GPIIb/IIIa-inhibitor MK383 inhibits thrombin generation in platelet rich plasma, suggesting an additional antithrombotic mechanism beyond platelet aggregation inhibition.
Answers are grounded in this paper and cite their sources.
Supports broader antithrombotic effects of GPIIb/IIIa inhibitors; leaves open clinical outcome validation.
Infusion of the GPIIb/IIIa-inhibitor MK383 inhibits thrombin generation in platelet rich plasma by interfering with the production of platelet procoagulant phospholipid exposure. The effect is similar to that of 0.2 U/ml of heparin. Heparin infusion, well known to inhibit thrombin generation by fostering antithrombin activity, inhibits the formation of platelet-derived procoagulant microparticles, probably by decreasing the formation of free thrombin, which, under our circumstances, is the main platelet activator.
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Keularts et al. (1998) studied this question. GPIIb/IIIa-inhibitor MK383 vs. Heparin (0.2 U/ml) was evaluated on Thrombin generation in platelet rich plasma. Infusion of the GPIIb/IIIa-inhibitor MK383 inhibited thrombin generation in platelet rich plasma to a similar extent as 0.2 U/ml of heparin.
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