Hyperplasminemia resulting from thrombolytic therapy exposes fibrinogen and other coagulation factors, plas-minogen, and a2-antiplasmin to nonspecific proteolysis by plasmin, a process normally regulated by a2-antiplas-min. Consumption of these factors and extensive fibrin dissolution leads to hemorrhage. The binding of plas-minogen to fibrin involves interactions with lysine-binding sites in plasminogen. These interactions are blocked by antifibrinolytic drugs such as aminocaproic acid (Amicar) and tranexamic acid (Cyklokapron); plasminogen activation primarily and plasmin prote-olytic activity are inhibited.
In addition to being an antidote to fibrinogenoly-sis during thrombolytic therapy, antifibrinolytic drugs are used orally and intravenously to control bleeding following surgery. They also are useful adjuncts to coagulation factor replacement during dental surgery in hemophiliac patients. Antifibrinolytic drugs are con-traindicated if intravascular coagulation is present. These drugs may cause nausea.
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