Open AccessThoughts on the Mechanism of Action of Aprotinin
Author(s) -
Royston David
Publication year - 2005
Publication title -
transfusion alternatives in transfusion medicine
Language(s) - English
Resource type - Journals
eISSN - 1778-428X
pISSN - 1295-9022
DOI - 10.1111/j.1778-428x.2005.tb00152.x
Subject(s) - aprotinin , medicine , fibrinolysis , mechanism of action , plasmin , mechanism (biology) , antifibrinolytic , coagulation , pharmacology , action (physics) , platelet , neuroscience , anesthesia , surgery , immunology , biochemistry , tranexamic acid , blood loss , chemistry , biology , epistemology , enzyme , in vitro , quantum mechanics , philosophy , physics
SUMMARY Currently there is no unifying theory that fully explains the hemostatic action of aprotinin. The majority of data related to the potential mechanism(s) of action of aprotinin can be broadly divided into the three topics of preservation of platelet function, reduced fibrinolysis and inhibition of thrombin generation. These three themes are not mutually exclusive and have evidence that either supports or refutes their importance in the process. What is clear when all of the scientific evidence is evaluated is that aprotinin is not simply an antifibrinolytic. The agent has multiple direct and indirect effects to inhibit platelet and coagulation functions in addition to inhibition of free plasmin. Despite the incomplete knowledge of its mechanism of action, aprotinin given in a sufficient dose remains the most potent agent currently available to prevent the need for transfusions of blood and hemostatic components in multiple surgical environments.