FORMATION OF THROMBI 323 



wliich may l)i' present in small numbers at the beginning, rapidly in- 

 crease in number, colleeting at the margins of the platelet masses and 

 between them. Not until the leucocytes have accumulated does the 

 fibrin appear. As Welch remarks, these findings afford no conclusive 

 evidence as to whether fibrin-ferment is formed from the leucocj^tes 

 or from the jilatelets, but since the fibrin does not appear until after 

 the leucocytes have accumulated, and also since small thrombi may 

 consist solely of platelets without fibrin, it seems probable that the 

 leucocytes must be looked upon as the chief source of the ferment. 

 If the blood is made ineoagulalile by injection of hirudin, injury to 

 the vessel-walls causes the formation of thrombi composed entirely of 

 platelets (Schwalbe). Sometimes small clots may form without the 

 apparent ])articipation of either platelets or leucocytes. These purely 

 fibrinous thrombi seem to start from injured endothelial cells, par- 

 ticularly in inflammatory conditions, such as pneumonic lungs, and 

 give the impression that the coagulin is derived from the endothelial 

 cells. Zurhelle attributes by far the most important part to the 

 platelets, an opinion shared by many, including Derewenko,^''' who 

 holds that the coagulation of blood with entirely occluded vessels is 

 quite distinct from true thrombosis because of the lack of platelets 

 in stagnant blood." Clots formed in the absence of platelets do not 

 shrink like proper thrombi fDuke). 



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 libera- 

 tion 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 re- 

 called that the joint action of tissue and blood coagulins is greater 

 than the sum of their individual actions, which also must be an im- 

 portant 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 uninjured vessel 

 may not result in thrombosis, and, on the other hand, extensive in- 

 jury or large calcified plaques in the intima of the aorta may also 

 cause no thrombosis because of the rapidity of the blood flow ; and, 

 furthermore, clotting may occur even in intact vessels under the influ- 

 ence of substances liberating fibrin-ferment in the blood; e. g., snake 

 venoms, nucleoprotein injections, and possibly in disease. As the red 

 corpuscles contain thromboplastic substances we may have thrombi 

 formed when hemolytic agents are present in relatively stagnant 



50 Ziegler's Beitj-., 1910 (48), 123. 

 5" Not accepted by Schwalbe, loc. cit. 



