The role of kininogenases, kinin formation and kininogenase inhibition in post traumatic shock and related conditions.

The kinin system has for a long time been considered to play a role in the pathophysiology of trauma, particularly in blood pressure changes and in inflammatory effects. Recent findings necessitate a revision of this view. It is now necessary to differentiate between two kinin systems: 1. the plasma kallikrein-HMW kininogen-kinin-system, which besides forming kinin acts decisively in Hageman Factor activation, clotting and fibrinolysis; 2. the glandular and tissue kallikrein-LMW kininogen-kinin-system which is to our present day knowledge primarily involved in kinin formation. Kinins exert a variety of actions. By interfering with angiotensin II formation, kinins may contribute to blood pressure regulation. By enhancing cellular glucose uptake and/or metabolism, they regulate partly energy production. In post traumatic states death is preceded by a severe depletion of various factors of the system and an almost total loss of kinin forming capacity. Severity and time course of these phenomena suggest that early institution of direct (Trasylol) or indirect (heparins, cortocosteroids) proteinase inhibition, and if necessary a replacement of the lost factors, should be considered.