COAGULATION NECROSIS 383 



of coagulation necrosis in infarcts, etc., as Weifrert maintained.^ 

 Schmaus and Albrecht believe that a true coagulation of the cell 

 proteins does occur in anemic infarcts, etc., for they found that the 

 cells of kidneys with lijrated vessels contain at first granules soluble 

 in water and salt solution; after forty-eight hours the granules cannot 

 be dissolved in these solvents or in weak acetic acid, but are soluble 

 in 2 per cent. KOH; after five to six days the granules are insoluble 

 even in KOH. Beyond these experiments, we seem to have no proof 

 of the occurrence of intracellular coagulation within areas of coagula- 

 tion necrosis due to anemia; exact chemical studies on this point are 

 much needed. Since tissue-cells contain coagulins for fibrinogen, it is 

 possible that they also contain coagulins for cell-proteins, but this 

 remains to be established. We do not know whether Chambers' 

 observations on the spontaneous coagulation of tiaumatized asteria 

 eggs^^o are applicable to other cells. Bacteria produce substances 

 coagulating milk and fibrinogen. Bergey^ calls attention to the 

 coagulation of serum by enzymes and acids produced by bacteria, 

 and RuppeP found that the tubercle bacillus produces substances 

 precipitating proteins; hence coagulation necrosis in bacterial infec- 

 tions may be brought about in this way, and SchmolP has shown 

 that the necrosis occurring in tubercles is associated with an almost 

 complete coagulation of the cell-proteins. 



Necrosis associated with inflammatory exudation is, of course, ac- 

 companied by coagulation of the fibrinogen of the exudate (e. g., 

 diphtheria); this type of coagulation necrosis is chemically a simple 

 fibrin-formation and readily understood. The peculiar hyaline de- 

 generations of parenchymatous cells (e. g., Zenker's degeneration 

 of muscles) are often included under this class, but it would seem 

 more probable that the processes consist rather of the fusion of the 

 structural elements of the cell into a homogeneous substance than a 

 true coagulation. When necrosis is produced by chemical means 

 more or less coagulation of some of the soluble proteins probably 

 takes place; even in plant cells this coagulation of dead protoplasm 

 is described.^ 



Liquefaction necrosis occurs particularly in the central nervous 

 system, where the cell substance seems not to undergo the coagulative 



^ Weigert believed that the dead area becomes permeated by plasma containing 

 fibrinogen, which is coagulated in and between the cells. He put much weight 

 on an increase in size of the necrotic area, which is by no means constant, as he 

 intimated; necrotic areas are inelastic, and when death occurs thej- do not shrink 

 with the fall of blood pressure as the surrounding tissues do, and hence they 

 may appear to project from the surface of the dead organ when thej- did not do 

 so during life. According to Moos (Virchow's Archiv., 1909 (195), 273) the plasma 

 does not permeate infarcted areas to the extent that Weigert assumed. 



3 Jour. Amer. Med. Assoc, 1907 (49), 680. 



* Zeit. phvsiol. Chem., 1898 (26), 218. 



6 Deut. Arch. klin. Med., 1904 (81), 163. 



^ Gaidukov. Zeit. chem. KoUoide, 1910 (6), 260; Lepeschkin, Ber. Deut. Bot. 

 Gesell., 1912 (30), 528. 



