32-1 DISTURBANCES OF CIRCULATION 



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 

 ^reas 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 

 blood, even without injury to the vessel-walls.^ Presumably the clot- 

 ting 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; 

 or, according to Howell's hypothesis, because the current brings an 

 excess of antithrombin to the point where the thromboplastin is being 

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

 current, and a high coagulability offer the most favorable conditions, 

 and we owe to Welch the appreciation of the fact that in a large pro- 

 rportion of all thrombi, even those caused by apparently purely me- 

 rchanical agencies (e. g., cardiac incompetence), bacteria are present 

 and probably determine the injury to the vessel-walls and the libera- 

 tion of fibrin-ferment.^ We have previously referred to L. Loeb's 

 . observations on the effect of bacteria in causing coagulation of the 

 blood. 



Hyalin thrombi are frequently the cause of extensive degenerative lesions in the 

 viscera, and although commonly formed of red corpuscles, they do not stain at all 

 like normal corpuscles, presumably because a certain proportion of the hemoglobin 

 has been altered or lost through hemolysis. Of particular interest is their reaction 

 to Weigert's fibrin stain, by which they often, but not always, stain intensely, 

 especially when hardened in Zenker's solution; a fact that has been the cause of 

 much confusion in earlier studies. Flexner* first appreciated the nature of these 

 thrombi as originating from agglutinated red corpuscles, although Hobs, 



6 Dietrich Cent. f. Path. (Verhandl.), 1912 (23), 372. 



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

 1900, vol. 15. 



8 Jour. Med. Research, 1902 (8), 316. 



