COAGULATION OF BLOOD 319 



disintegration, nnicli as other antienzymes are supposed to act in 

 prevontins autodigcstion of living cellp. 



Coagulation of drawn blood may be retarded experimentally by re- 

 moval of the calcium by precipitation as oxalate, fluoride, etc.; also by 

 diminishing the oxygen and increasing the COi,, by addition of solu- 

 tions of neutral salts in large amounts, by diluting greatly with water, 

 or by keeping the blood cold. Bile salts retard coagulation markedly, 

 by interfering with the conversion of fibrinogen into fibrin." Coagu- 

 lation may be hastened by moderate heat, by whipping, exposure to 

 air, by contact with much foreign matter, and by the addition of 

 watery extracts from many different tissues and organs. Poisons that 

 destroy the platelets reduce the coagulation (Duke). Of particular 

 interest pathologically is the retardation of coagulation that follows 

 injections of proteoses (the so-called "peptone" solutions) and also 

 various other protein-containing solutions, such as organ extracts, 

 bacterial toxins, snake venoms, eel serum, extract of leeches or of 

 Uncinaria, impure nucleo-protein solutions, or solutions of various 

 colloids. Most of these substances e. g., peptone, eel serum, cause 

 reduction of coagulability when injected into animals, and are without 

 effect on blood removed from the body. A few, however, prevent 

 coagulation of drawn blood (snake venom, extract of leeches). When 

 substances of the first class are injected in sufficient quantities, there 

 occurs first a period of accelerated coagulation which may, particularly 

 in the case of organ extracts, cause prompt death from intravascular 

 clotting; if the animal survives, there follows a period of decrease 

 or total inhibition of coagulability of the blood, both within the ves- 

 sels and after removal from the body. The first period of increased 

 coagulability undoubtedly depends upon the formation of a large 

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

 plained 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, a view which is receiving much support 

 from recent observations. According to Davis"" injection of tlirombin 

 is followed quickly by an increase in the amount of antithrombin in the 

 blood. It has been found that in animals deprived of the liver no 

 coagulation-inhibiting substances are formed in the blood after in- 

 jection of proteoses, hence Delezenne believes that the substances of 

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



" Haessler and Stebbins, Jour. Exp. Med., 1919 (29), 445. 

 "«Amer. Jour. Physiol., 1911 (29), IGO. 



