270 DISTURBANCES OF CIRCULATION 



injured endothelial cells, particularly in inflammatory conditions, 

 such as pneumonic lungs, and give the impression that the 

 coagulin is derived from the endothelial cells. 



The process of clotting in the stoppage of hemorrhage offers 

 some differences from intravascular clotting, in that the 

 coagulins of the tissue-cells also come into play. It is rather 

 difficult to determine how much of the coagulation depends on 

 these, and how much on the coagulins of the leucocytes, for the 

 same conditions that favor liberation of tissue coagulins, i. e., 

 much laceration and destruction of the tissue, also favor the 

 disintegration of leucocytes by offering large areas of surface 

 for contact. Loeb is of the opinion, however, that of the two, 

 the latter factor is the more important. It may be recalled that 

 the joint action of tissue and blood coagulins is greater than the 

 sum of their individual actions, which also must be an important 

 factor in causing clotting in bleeding wounds. 



As to the relative importance of stagnation and vessel injury 

 in producing thrombosis, we know that total stasis in an unin- 

 jured vessel may not result in thrombosis, and, on the other 

 hand, extensive injury or large calcified plaques in the intima 

 of the aorta may also cause no thrombosis because of the rapid- 

 ity of the blood flow ; and, furthermore, clotting may occur even 

 in intact vessels under the influence of substances liberating 

 fibrin-ferment in the blood ; e. g., snake venoms, nucleoproteid 

 injections, and possibly in disease. Presumably clotting does 

 not occur when the stream is rapid, because any fibrin-ferment 

 that may be liberated by injured leucocytes or endothelium is 

 swept away before fibrin can become attached to the vessel- wall. 

 Naturally the combination of an injured vessel- wall, a slow cur- 

 rent, and a high coagulability offer the most favorable condi- 

 tions, and we owe to Welch the appreciation of the fact that in a 

 large proportion of all thrombi, even those caused by apparently 

 purely mechanical agencies (e. g., cardiac incompetence), bac- 

 teria are present and probably determine the injury to the 

 vessel-walls and the liberation of fibrin-ferment. 1 We have 

 previously referred to L. Loeb's observations on the effect of 

 bacteria in causing coagulation of the blood. 



Hyaline thrombi have become of particular interest during 

 the past few years, since it has been shown that they are fre- 

 quently the cause of extensive degenerative lesions in the vis- 

 cera, and also because of their relation to the more recently 

 understood Jiemagglutinating substances (see Chap. ix). Although 



1 Welch, Venous Thrombosis in Cardiac Disease, Trans. Assoc. Amer. Phys., 

 1900, vol. 15. 



