320 DISTURBANCES OF CIRCULATION 



similar substances may well play a part in affecting coagulation in 

 infectious diseases, and Whipple ^' has found a decreased coagula- 

 bility in sei)ticemia because of the })resence of an excess of anti- 

 thrombin. It may also be mentioned that animals soon acquire an 

 immunity against proteoses, so that their inhibiting influence is no 

 longer shown. This corresponds to the observation of Kanthack ^^ 

 that immune serum against venom, neutralizes very effectively the 

 anticoagulating principle of venom ; an amount of antiserum alto- 

 gether insufficient to neutralize the toxic properties of venom will 

 neutralize its property of preventing clotting. The bacterial prod- 

 ucts may also modify coagulation, and L. Loeb '" has found that 

 different organisms are unequally effective in this respect, Staphylo- 

 coccus aureus being much more powerful in causing coagulation than 

 any others tested ; *° typhoid, diphtheria, tubercle, and xerosis bacilli 

 and streptococci being without any apparent effect, while pyocyan- 

 eus, prodigiosus. and colon bacilli occupy an intermediate position. 

 Furthermore, after the organisms are killed by boiling, this effect is 

 greatly reduced, showing that it does not depend merely upon the 

 mechanical action of the bacteria, but probably upon bacterial prod- 

 ucts contained in the culture-media. 



After phosphorus-poisoning the blood may become non-coagulable, 

 which Jacoby *^ ascribed to an absence of fibrinogen in the blood, be- 

 cause of a fibrinogen-destroying ferment in the liver. Doyon *- has 

 made a similar finding in chloroform necrosis of the liver, but he at- 

 tributes especial importance to an excess of antitlirombin liberated 

 from the liver in these conditions. Whipple has also found a de- 

 crease in fibrinogen with chloroform necrosis and cirrhosis of the 

 liver.*-'' In other instances of decreased coagulability the fibrinogen 

 is present, generally in normal amounts. After death the blood be- 

 comes incoagulable because the fibrinogen is destroyed through a 

 process similar to that of fibrinolysis; *^ this fibrinolysis may be com- 

 plete as early as ten hours after death. The other proteins of the 

 blood do not seem to be corresi)on(lingly attacked. Thrombokinase 

 is also scanty in cadaver blood, but there seem to be no coagulation- 

 inhibiting substances present. In anaphylactic shock the coagula- 

 bility is reduced or abolished, associated wath which is a leucopenia.** 



37 Arch. Int. Med.. 1012 (9), 305. 

 -« Cited by La/.anis-Barlow, p. 141. 

 30 .Tour. Med. Hesearcli, \'M):\ (10), 407. 



41 ]\Tueli (Biocliem. Zeit., 1!»0S (14), 14:5) states that stai>hyloeoeeus oontains 

 tlirf)nit)()kinase. 



•»i Zeit. phvsiol. Chem., 1000 (30), IT;")-, also Doyoii rt a]., Compt. Bend. Soc. 

 Biol., 1005 (58), 403. 



42 Compt. Bend. Soc. Biol., 1005 (58), 704; .lour, piiys. et path., 101-2 (14), 

 229. 



42a P.ull. .lohna Hopkins Ilosp., 1013 (24). 207. 



43 Morawitz, Hofmeister's Beitr., lOOf, (8). 1. 



44 The ineoagulaliility of menstrual blood is ascribed to a lack of lilirin ferment 



