VAIUETlEii OF \ECltOSIS 381 



b}^ causing structural alteration in the cell (c. <j., the bursting; of 

 plant-cells in water), or concentration of the electrolytes may become 

 so great that the colloids are thrown out of solution, as in the ordi- 

 nary salting-out processes of the laboratory. It is doubtful, however, 

 if osmotic changes per se ever become so abnormal within the animal 

 body (except in experimental conditions) as of themselves to cause 

 cell necrosis. 



VARIETIES OF NECROSIS 



Coagitlation Necrosis.''" — This name is applied to necrotic areas 

 that are lirni, dry, usually pale yellowish in color, and observed prin- 

 cipally in areas of total anemia or tuberculosis. The question has 

 been long disputed as to whether a true coagulation occurs in such 

 tissues or not. Necrosis produced by heat, carbolic acid, corrosive- 

 sublimate, etc., is naturally a coagulation necrosis, the cells of the 

 att'ected area having undergone true coagulation ; i. e., the conversion , 

 of their soluble colloids {sols) into the insoluble ''pectous" modifica- 

 tion. Whether the same change occurs in areas of anemic necrosis 

 is not so well established. If the part contains a fair amount of 

 plasma the liberation of the tissue coagulins from the dead cells will 

 cause a conversion of the fibrinogen into fibrin — this can usually be 

 demonstrated microscopically, but the presence of fibrin is not con- 

 stant, and its quantity is usually insufficient to explain satisfactorily 

 the condition of coagulation necrosis in infarcts, etc., as Weigert 

 maintained."^ Sclimaus and Albrecht believe that a true coagula- 

 tion of the cell proteins does occur in anemic infarcts, etc., for they 

 found that the cells of kidneys with ligated 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 coagulation 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 coag- 

 ulins for cell-proteins, but this remains to be established. Bacteria 

 produce substances coagulating milk and fibrinogen. Bergey '''* calls 

 attention to the coagulation of serum by enzymes and acids produced 



67 Literature J)y Jores, Ergebnisse der Pathol., 180S (5), 16. 



68 Weigert believed that the dead area becomes permeated by plasma eontainiiig 

 fibrinogen, which is coagulated in and between the cells. lie put much weiglit 

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

 i-itimated; necrotic areas are inelastic, and when death occurs tliey do not 

 shrink with the fall of lilood juessure as the surrounding tissues do, and lience 

 they may appear to project from the surface of the dead organ Mlien tiiey did 

 not do so dviring life. According to Moos (Virchow's Archiv., l!)On (10.5) , 27.'}) 

 the plasma does not permeate infarcted areas to the e.xtent that ^Yeigert assumed. 



fisJour. Amer. Med. Assoc., 15107 (40), G80 



