Abstract
Plasma has been shown to contribute to fibrinolysis in vitro by plasminogen activator activities from tissue-type plasminogen activator, from urokinase-type plasminogen activator and from a factor XII-dependent pathway. The aim of the present study was to further outline the activation route for factor XII-dependent fibrinolysis. To this end effects of purified active enzymes added to dextran sulphate euglobulin fractions of plasma's deficient in factor XII (Hageman trait) or prekallikrein (Fletcher trait) were studied. In Hageman and Fletcher trait plasma, the activation of factor XII-dependent activator activity could be corrected by the addition of the activated factor, kallikrein. Activated, β-factor XIIa was only effective in Hageman trait plasma. Additions of plasmin, tissue-type plasminogen activator or urokinase-type plasminogen activator were not effective in Hageman trait plasma. It is concluded that factor XII-dependent plasminogen activator activity is generated predominatly via kallikrein.
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