Platelet anti-aggregant and rheological properties of piracetam. A pharmacodynamic study in normal subjects.
Moriau M, Crasborn L, Lavenne-Pardonge E, von Frenckell R, Col-Debeys C.
Department of Internal Medicine,
University of Louvain (UCL),
St.-Luc University Clinics, Brussels, Belgium.
Arzneimittelforschung 1993 Feb;43(2):110-8
The random administration of four different single oral doses of piracetam (1.6 g, 3.2 g, 4.8 g and 9.6 g–at fixed intervals of 2 weeks to 5 healthy subjects has confirmed and explicited its platelet anti-aggregant and rheological properties after doses of 4.8 g and 9.6 g. The effect on platelet aggregation occurs through inhibition of thromboxane synthetase or anti-thromboxane A2 activity together with a reduction in the plasma level of von Willebrand’s factor (F.VIIIR:vW). The rheological effect is related to the action of piracetam on cell membrane deformability (red cells, white cells and platelets) and to its simultaneous effect in reducing by 30-40% plasma levels of fibrinogen and von Willebrand’s factor. In addition, it exerts a direct stimulant effect on prostacyclin synthesis in healthy endothelium. These effects are greatest between 1 and 4 h after dosage, and then diminish progressively to disappear between 8 and 12 h after administration. This explains the need to divide the total daily dose into 3 intakes at 8-hourly intervals. This study confirms the presence of four sites of action of piracetam: the vessel wall, platelets, plasma and cell membranes (RBC, WBC), which provide the basis for the potentially important anti-thrombotic activity of piracetam.