<unk>  (simplified). Blue arrows denote stimulation, and red arrows inhibition. Plasmin is produced in an inactive form, plasminogen, in the liver. Although plasminogen cannot cleave fibrin, it still has an affinity for it, and is incorporated into the clot when it is formed. Tissue plasminogen activator (t-PA) and urokinase are the agents that convert plasminogen to the active plasmin, thus allowing<unk>  to occur. t-PA is released into the blood slowly by the damaged endothelium of the blood vessels, such that, after several days (when the bleeding has stopped), the clot is broken down. This occurs because plasminogen became entrapped within the clot when it formed; as it is slowly activated, it breaks down the fibrin mesh. t-PA and urokinase are themselves inhibited by plasminogen activator inhibitor-1 and plasminogen activator inhibitor-2 (PAI-1 and PAI-2). In contrast, plasminogen further stimulates plasmin generation by producing more active forms of both tissue plasminogen activator (tPA) and urokinase. α2-Antiplasmin and α2-macroglobulin inactivate plasmin. Plasmin activity is also reduced by thrombin-activatable<unk>  inhibitor (TAFI), which modifies fibrin to make it more resistant to the tPA-mediated plasminogen.
Fibrinolysis
Thrombolysis
Argon plasma coagulation
Prothrombin complex concentrate
Thrombectomy
Tissue plasminogen activator
Low-molecular-weight heparin
Tinzaparin sodium