COAGULATION OF THE BLOOD 267 



of coagulability of the blood, both within the vessels and after 

 removal from the body. The first period of increased coagula- 

 bility undoubtedly depends upon the formation of a large amount 

 of fibrin-ferment, but it has not yet been satisfactorily explained 

 how the inhibition of coagulation is produced. Apparently the 

 fibrin-ferment formed at first is rapidly destroyed, but it is 

 thought by some that it is converted into a substance that 

 neutralizes the fibrin-ferment that may be formed later, or that 

 a true anticoagulin is formed. It is also among the possibilities 

 that all the available prothrombin or thrombokinase is used up 

 during the first stage of acceleration. As before mentioned, the 

 blood and tissues contain substances that inhibit coagulation, and 

 it may be that these are secreted in excessive amounts. It 

 has been found that in animals deprived of the liver no coagu- 

 lation-inhibiting substances are formed in the blood after injec- 

 tion of proteoses, hence Delezenne believes that the substances 

 of this class act by causing a destruction of leucocytes, thus 

 liberating a substance which increases coagulation and also 

 another substance retarding coagulation ; the first of these is 

 destroyed by the liver, leaving the retarding substance to act 

 unopposed. 1 Leech extract (hirudiri) prevents clotting by means 

 of an antiferment action, combining with the thrombin. Snake 

 venom, however, acts upon the thrombokinase (Morawitz). 



Coagulability of the Blood in Disease. In disease 

 the alterations in the coagulability of the blood depend upon 

 much the same factors. The high coagulability in lobar pneu- 

 monia is undoubtedly caused, at least in part, by an excessive 

 formation of fibrin-ferment through the extensive disintegration 

 of leucocytes. In all conditions associated with suppuration 

 and leucocytosis the amount of fibrinogen is also increased. 

 The fluidity of the blood in septicemia is probably dependent 

 upon the appearance of the coagulation-inhibiting phase that 

 follows the action of the products of cell destruction, including 

 among them proteoses. In this connection should be mentioned 

 the observation of Conradi, 2 who found that among the products 

 of autolysis is a coagulation-inhibiting substance which is not 

 destroyed by heat, diffuses readily, and in general behaves unlike 

 the proteids. This or similar substances may well play a part 

 in affecting coagulation in infectious diseases. It may also be 

 mentioned that animals soon acquire an immunity against 



1 The manner in which gelatin injections cause an increase in the blood 

 coagulability is not yet understood (see Boggs, Deut. Arch. klin. Med., 1904 

 (79), 539). 



2 Hofmeister's Beitr., 1901 (1), 137. 



