Aspirin, indomethacin and dazoxiben do not affect the fibrinolytic activation induced by venous occlusion.
A cause-effect relation between the synthesis and release of prostaglandins and fibrinolytic activation has been suggested. We have reinvestigated this relation in a double-blind, placebo-controlled, cross-over study with cyclooxygenase inhibitors (aspirin and indomethacin) and a thromboxane synthase inhibitor (dazoxiben) in nine healthy volunteers. Euglobulin fibrinolytic activity (EFA) and tissue-type plasminogen activator antigen level (t-PA:Ag) were studied before and after 10 min of venous occlusion. Despite effective suppression of prostaglandin synthesis by aspirin and indomethacin and enhanced prostacyclin formation by dazoxiben, baseline EFA and t-PA:Ag levels did not significantly change within 2 hours after ingestion of the different drugs. The release of t-PA by venous occlusion was not altered by any of the drugs. Thus, our study does not support the hypothesis that prostaglandins play a significant role in the modulation of the synthesis or release of t-PA.
D001241:Aspirin / Q000494:pharmacology*; D004311:Double-Blind Method; D005342:Fibrinolysis / Q000187:drug effects*; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology*; D007213:Indomethacin / Q000494:pharmacology*; D008297:Male; D011453:Prostaglandins / Q000502:physiology*; D012712:Serum Globulins / Q000502:physiology; D010959:Tissue Plasminogen Activator / Q000032:analysis; D014652:Vascular Diseases / Q000097:blood; D014680:Veins
D007093:Imidazoles; D011453:Prostaglandins; D012712:Serum Globulins; C029166:dazoxiben; D010959:Tissue Plasminogen Activator; D001241:Aspirin; D007213:Indomethacin