Abstract
Conclusions
There is no valid reason to suppose that the fundamental process of thrombin formation differs as between the phos-pholipid and the enzymic modes of activation. 2 The fact of the significant quantitative differences in the cited tests shows that the so-called “antiprothrombic” effect of heparin is not to be interpreted as an alteration of the prothrombin itself, but rather as a manifestation of antagonisms between the heparin and the thromboplastic factors. There is an experimental difference between the simple addition of cephalin and its enzymic mobilization from protein-phospholipid combinations.
The results of all clotting experiments must be evaluated with reference to (1) quantitative relationships between the various factors, (2) the question of cephalin mobilization, and (3) time factors involved in thrombin formation, the thrombin-fibrinogen interaction, and in the overcoming of the inhibitory mechanisms. It is significant that thromboplastic enzyme has demonstrable powers of overcoming the “antiprothrombic” inhibitory mechanisms. The “antithrombic” action of heparin-albumin mixtures is immediately evident and is not dependent upon the type of thromboplastic agent used in the preparation of the thrombin.
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