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The effect of acetylsalicylic acid in 3 different formulations on in vitro and in vivo platelet function tests. An experimental study on healthy male volunteers.

The template bleeding time (TBT), ADP-induced platelet aggregation, and serum production of TXB2 were measured in healthy young male subjects immediately before, and on days 1, 4 and 6 after the ingestion of 1 single dose of 500 mg acetylsalicylic acid (ASA) in 3 different formulations: Aspirin (Bayer), and the 2 enteric-coated formulations Reumyl (Hässle) and Premaspin (Lääke). The ingestion of Aspirin resulted in a significant prolongation of the TBT over a period of 6 d. However, after the ingestion of the same amount of ASA in the 2 enteric coated formulations, the TBT as measured on day 6 had become normalized. After the ingestion of Aspirin, there was no reappearance of the second wave of ADP-induced platelet aggregation during the study period; however, after the ingestion of the 2 enteric-coated formulations, secondary platelet aggregation occasionally returned on day 6. In response to the intake of each of the 3 ASA formulations, the serum TXB2 production as measured 24 h later was almost completely inhibited. In each of the 3 study groups, the TXB2 formation as measured on day 6 was still significantly impaired.

Adult↗

Changes of 32P-incorporation in vitro into phospholipids of blood platelets after whole-body irradiation of rabbits. I. Comparison of 32P-incorporation with some platelet functional tests during early development of postirradiation thrombocytopenia.

In the period of postirradiation bone-marrow activity depression, changes of the 32P incorporation into phospholipids of blood platelets in rabbits after whole-body exposure to 103.2 mC/kg were noted in vitro. Increased incorporation into phosphatidylcholine, phosphatidylethanolamine and sphingomyeline on the 11th day and into phosphatidylserine on the 8th and 11th day were recorded. On the 5th, 8th and 11th days the pattern of incorporation is changed. During this period a pronounced decrease of 32P incorporation into phosphatidylinositols of the blood platelets was noted, no changes in the representation of the phospholipids of interest (PC, PE, SM, PS, PI) were observed and no alterations of the blood platelet adhesiveness were found. The PF3-A and PF3-F test did not reveal any significant changes of the role of PF 3 in the blood clotting process.

Animals↗