Title : Increased urokinase and consumption of α2 -antiplasmin as an explanation for the loss of benefit of tranexamic acid after treatment delay.

Pub. Date : 2019 Jan

PMID : 30451372






5 Functional Relationships(s)
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Compound Name
Protein Name
Organism
1 Urokinase + tranexamic acid produces plasmin in plasma or blood and disrupts clotting. Tranexamic Acid plasminogen Homo sapiens
2 Results IC50 values for antifibrinolytic activity of TXA varied from < 10 to > 1000 mumol L-1 depending on the system, but good fibrin protection was observed in the presence of tPA, uPA and plasmin. Tranexamic Acid plasminogen Homo sapiens
3 However, in plasma or blood, active plasmin was generated by TXA + uPA (but not tPA) and coagulopathy developed leading to no or poor clot formation. Tranexamic Acid plasminogen Homo sapiens
4 Conclusions Tranexamic acid protects fibrin but stimulates uPA activity and slows inhibition of plasmin by alpha2 -antiplasmin. Tranexamic Acid plasminogen Homo sapiens
5 Additional direct inhibition of plasmin by aprotinin may prevent development of coagulopathy and extend the useful time window of TXA treatment. Tranexamic Acid plasminogen Homo sapiens