| Research Abstract |
By measuring platelet surface P-selectin as a marker of platelet activation, the activation effects of tissue-type plasminogen activator and urokinase and the inhibitory effects of acetylsalicylic acid were investigated. After addition of urokinase (final concentration : 192 U/ml, 1,920 U/ml, or 19,200 U/ml) or tissue-type plasminogen activator (final concentration : 120 U/ml, 1,200 U/ml, or12,000 U/ml) to platelet-rich plasma from 12 healthy individuals, platelet-rich surface P-selectin expression was measured by flow cytometry using an anti-CD62 monoclonal antibody. Urokinase and tissue-type plasminogen activator increased platelet surface P-selectin expression in a concentration-dependent manner. Next, either 160 mg/day (n=6) or 660 mg/day (n=6) of acetylsalicylic acid were administered to the 12 healthy individuals, and venous blood samples were collected after 7 days of treatment. Platelet surface P-selectin expression was then measured by the same method before and after addition of tissue-type plasminogen activator or urokinase. Although the effect of acetylsalicylic acid at 160 mg/day on P-selectin expression was minimal, a dose of 660 mg/day supressed platelet surface P-selectin expression significantly and also significantly inhibited the platelet activating effects of tissue-type plasminogen activator and urokinase. From these findings, it was concluded that platelets were activated by tissue-type plasminogen activator or urokinase, and that platelet activation could be supressed by administering acetylsalicylic acid at 660 mg/day.
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