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Arch Intern Med (Chic). 1942;69(4):647-661. doi:10.1001/archinte.1942.00200160098008.
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The failure of the circulating blood to clot spontaneously under physiologic conditions in vivo still remains a unique and obscure phenomenon, since all of the elements essential for immediate coagulation in vitro are apparently present. Howell, in his fundamental concept of blood coagulation, has consistently maintained in at least partial explanation of this enigma that substances acting as clotting inhibitors are normally present in blood plasma. With the identification of heparin by Howell and Holt1 and the demonstration of the presence of proantithrombin, the nature and role of these anticoagulants in the blood began to be better understood. Evidence has been presented suggesting that the principal anticoagulant effect of heparin is the prevention of the conversion of prothrombin to thrombin. However, when added to plasma, heparin apparently activates the proantithrombin, resulting in a tremendous increase in antithrombic activity. Charles and Scott,2 among others, have confirmed the presence of


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