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  • Title: Plasma concentrations and anti-platelet effects after low dose acetylsalicylic acid.
    Author: Rosenkranz B, Frölich JC.
    Journal: Prostaglandins Leukot Med; 1985 Sep; 19(3):289-300. PubMed ID: 3864170.
    Abstract:
    The present study has investigated whether low-dose acetylsalicylic acid (ASA) can inhibit platelet aggregation locally at its site of gastrointestinal absorption without concentrations in the systemic circulation high enough for inhibition of cyclooxygenase. For this purpose platelet aggregation, thromboxane formation as well as ASA plasma concentrations were measured in 8 volunteers before oral intake of 100 mg ASA as well as 20 to 300 minutes thereafter. At each time 5 ml of blood were mixed with 5 ml of blood obtained from a second, untreated volunteer. Aggregation and thromboxane formation were also determined in these mixed blood samples. The same protocol was performed with 4 volunteers after administration of 1500 mg ASA as well as after no drug intake. In a separate experiment the concentration-effect-relationship of ASA was assessed in vitro. One hundred and forty minutes after administration of 100 mg ASA aggregation and thromboxane formation were significantly decreased to 49.4 and 4.5% of the initial values, respectively, whereas in the mixed blood sample aggregation was not impaired. Inhibition of thromboxane formation was constantly 73% of the inhibition observed in the unmixed sample throughout the study period and thus most probably was caused by dilution of the platelets of the untreated volunteer by the inactivated platelets of the ASA-treated volunteer. These data suggest the absence of pharmacologically active drug concentrations in the peripheral blood. ASA plasma concentration was highest after 40 minutes (2.2 +/- 1.6 microgram/ml; n = 5). After the 1500 mg ASA dose platelet function and thromboxane formation decreased to 29.8 and 2.0% of the initial values, respectively. Furthermore, aggregation and thromboxane formation in the mixed blood sample were markedly reduced. Thus, after the high dose of ASA effective plasma concentrations were present in the peripheral circulation. Highest ASA plasma concentrations were 21.1 +/- 8.9 micrograms/ml. IC50 values were 1.00 +/- 0.36 and 0.30 +/- 0.05 microgram/ml for aggregation and thromboxane formation in vitro, respectively. It is concluded that low dose ASA can effectively inhibit platelet function without producing pharmacologically active concentrations in the peripheral circulation.
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