Abstract
In health, steady state levels of factor X (FX), factor II (FII), antitnrombin III (AT3) and alpha-2 macroglobulin (A2M) are determined by synthetic and physiologic breakdown rates. Wnen FX is activated, FXa and thrombin react with AT3 and A2M bimolecularly to form complexes. In steady states simple relations define the resulting increased consumption of FX, FII, AT3 and A2M and plasma levels of free FXa and thrombin. FXa varies as ∼1/(AT3 level) and thrombin as ∼1/(AT3 level) 2. This explains the susceptibility to thrombosis of patients with relatively moderately reduced AT3 levels. The same equations show that neparin and coumarin act multiplicatively to reduce thrombin levels and that neparin inhibits the sparing of AT3 by other antiproteases. Effects of activation of factor IX and modification of reactants by distribution in different blood phases are briefly noted.
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