The effects of aprotinin on the contact pathway are dependent on the circulating plasma concentrations (expressed as kallikrein inactivation units (kIU) per milliliter) since the affinity of aprotinin for plasmin is significantly greater than that for plasma kallikrein ( Fritz..a.Dd..Wu.Dd.ei®Ll983). At a plasma level of 125 kIU/ml aprotinin inhibits fibrinolysis and complement activation. Inhibition of plasma kallikrein requires higher doses to provide plasma levels of 250 to 500 kIU/ml.
1. Plasma kallikrein inhibition reduces blood coagulation mediated via contact with anionic surfaces and, in the critically ill patient, improves circulatory stability via reduced kinin activation.
2. Prevention of inappropriate platelet activation: neutrophil activation (mediated by complement or kallikrein) causes a secondary activation of platelets. The release of cathepsin G from neutrophil granules is important in this platelet-neutrophil interaction. It has recently been demonstrated that aprotinin can significantly inhibit the platelet activation due to purified cathepsin G; this mechanism forms a direct inhibition of inappropriate neutrophil-mediated platelet activation.
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