Tiii{(> ]fiiosis 315 



trated blood of passive congestion the corpuscles may number six to 

 eight millions per .cubic millimeter, while the concentration of the 

 solids of the serum may be at tlie same time reduced CKrehl). The 

 viscosity of such blood is higher than that of normal l)lood.^* In 

 acute stasis the proi)orti()n of serum proteins, especially the albumin, 

 increases with the duration of the stasis ; no changes occur in the non- 

 protein constituents of the blood (Rowe).^^^ 



THROMBOSIS 



The cliemistry of thrombosis in most respects resolves itself into the 

 chemistry of fibrin formation, a subject which is so extensively con- 

 sidered in most treatises on physiological chemistry and physiology 

 that it does not seem desirable to give here anything more than the 

 essential principles involved in the clotting of the blood, as now under- 

 stood, as an introduction to the consideration of the same process as 

 it occurs under pathological conditions. In spite of innumerable in- 

 vestigations, our knowledge of the actual participants and processes 

 involved in the formation of fibrin is in a veiy unsatisfactory and 

 fragmentary state. Some facts seem well established, however, and 

 we have a general idea of the subject that may be applied with ad- 

 vantage to the consideration of thrombosis. 



FIBRIN FORMATION.i- 



Several difFeront substances seem to l)e eoneerned in the forniation of fibrin, 

 of -which tlie first of importance is its antecedent, fibrinogen. Fibrinogen is a 

 simple protein, related to the globulins, and diflfering chiefly in its icady coagula- 

 bility, not only by fibrin ferment, but also by heat, salts, and other coagulating 

 agencies. By itself, however, it shows no tendency to coasrulate spontaneously. 

 According to Goodpasture.ifi fibrinosen is formed through tlie combined activity 

 of the liver and intestines, although earlier writers have, variously described its 

 formation in the bone marrow, leucocytes, liver or intestines. The amount of 

 fibrinogen present in the blood is actually quite small, the fibrin formed in nor- 

 mal clotting being but 0.1 to 0.4 per cent, of tlie weiffht of the blood. Acted 

 upon by the fibrin-ferment, it yields the characteristic insoluble protein fibrin, in 

 crystalline form under favorable conditions,!" but we do not know definitely what 

 changes the fibrinogen undercroes in this process. Fibrin resembles in its insolu- 

 bility the proteins coagulated by heat, alcohol, etc., but when kept aseptically for 

 some time, it becomes asain dissolved; this process of fibrinoh/sis probably de- 

 pends upon proteolytic enzymes, which fibrin, in common with other sulistances 

 of similar physical nature, has the property of dragging out of solution and 

 holding firmly. Undonljtedly entangled leucocytes are also an important factor 

 in the fibrinolysis. lo which is greatly increased in phosphorus poisoning and when 

 the liver is excluded from the circulation, a fact suggesting that tlie liver may 

 form inhibiting substances. 



i4Determann. Zeit. klin. :Med.. inOO (.5n), U. 2-4. 



14a .Tour. Lab. flin. :\fed., 1016 (1), 48.5. 



15 For literature and full discussion see Hammarsten's or ^lathews' Physiolog- 

 ical Chemistry; ;Morawitz, Ergebnisse der Phvsiol., Abt. 1, 1004 (4), 307. and 

 the andbuch "d. Biochem., 1008 II (2), 40; 'Leo Loeb, Biochem, Centr.. 1907 

 (6), 829. 



ifi Amer. Jour. Physiol., 1914 (3.3), 70. 



1' See Howell. Amer. Jour. Phvsiol., 1014 (3.5), 143; Hekma, Internat. Zeit. 

 physik. chem. Biol., 191.5 (2), 279. 



19 See Morawitz, loc. cit.; also Pvulot, Arch, internat. d. Physiol.. 1904 (1), 152. 



