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The pharmacokinetic-pharmacodynamic model for ascertaining the antiplatelet effect of aspirin was developed, considering the effect of aspirin on the metabolic turnover of cyclooxygenase in platelets and vessel wall endothelium. All date used for analysis were obtained from the literature. The pharmacodynamic parameters, K, K', ke and ke' as reaction rate constants of aspirin and cyclooxygenase in platelets and that in endothelium, and the turnover rate constants of cyclooxygenase in platelets and that in endothelium, respectively, were calculated based on the plasma aspirin concentration profile, the plasma thromboxane B2 concentration as the index of inhibition of cyclooxygenase in platelets and the reduction of prostacyclin production of venous tissue as the index of inhibition of cyclooxygenase in vessel wall endothelium.The values of K and K' were 3.21 and 0.97 ml·μg-1 · hr-1, respectively, demonstrating selectivity of aspirin to cyclooxygenase in platelets. The value of ke was 0.00630 hr-1, which was consistent with the platelet life span. The developed model could explain the long duration of antiplatelet activity of aspirin and may be useful for formulating a rational dosage regimen for effective antiplatelet therapy utilizing aspirin.

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Parmacodynamic Analysis of Antiplatelet Effect of Aspirin in the Literature. Modeling Based on Inhibition of Cyclooxygenase in the Platelet and the Vessel Wall Endothelium.