AUTO/ASIS J\ l> \Tlli)l.<)(;i(\L I'mx'EfSFfEH 91 



iilbuinin to catgut ligatures. 'I'lic lictci-olysis iiuiy be iutracellular 

 ■\vliou the material to be digested luis tirst beeu taken up by the cells 



(phagocytosis) ; or extra-cellular, either by enzymes normally con- 

 tained in the blood ])lasma and tissue fluids, or by enzymes liberated 

 by the leucocytes and tixed tissue cells. On death and dissolution of 

 a cell the intracellular enzj'mes are released,'*"^ but it is not known to 

 what extent the enzymes may be secreted from intact living cells. As 

 far as pathological processes show, the amount of liberation of en- 

 zymes from normal cells is very slight, if any, and the digestive en- 

 zymes of the blood plasma seem to be very feeble, but this is perhaps 

 because they are largely held in check by the anti-enzymatic substances 

 of the serum. I'athological autolysis and heterolysis, therefore, are 

 brought about chiefly by enzymes liberated from dead or injured cells. 

 Bacteria, however, can multiply upon a medium of coagulated protein, 

 M'hich suggests that they also secrete proteolytic substances, for other- 

 wise it would be difficult to explain how they secure their nourish- 

 ment. In pathological conditions, digestion of degenerated tissues 

 seems usually to be the result of both autolysis and heterolysis. An 

 infarct softens because the intracellular enzymes digest the dead cells, 

 exactly as they do when the tissue is removed from the body, ground 

 up, and put in the incubator under toluene. In addition leucocytes 

 wander in, disintegrate, and their liberated enzymes help in the proc- 

 ess, as also do, to a less degree, the enzymes of the blood plasma. It is 

 because of the heterolysis by leucocytic enzymes that a septic infarct 

 becomes softened so much more rapidly than does a sterile infarct, and 

 by comparing the rate of softening in septic and aseptic infarcts we 

 see that the cellular autolysis is a very slow process as compared to 

 the heterolysis accomplished by the leucocytes. The explanation of 

 this may lie in the fact that most intracellular proteases act best in 

 an acid medium (Wiener), while leucocytic proteases act best in an 

 alkaline medium (Opie), and the infarcts of small size are seeped 

 through by alkaline blood fluids. When an infarct is large, we find 

 it undergoing central softening while the periphery remains firm ; this 

 corroborates our hypothesis, for acids are developed during autolysis 



(Magnus-Levy), which at the periphery are neutralized by the blood 

 plasma, so that only at the center is autolysis active. The inhibiting 



formed by the leuooevte itself. Opie (Jour. Exp. ^led., 10(1.7 (7). T.IO ) Juis shown, 

 liowever. that the bone-marrow contains proteolytic enzymes which are like those 

 of the leucocytes in that tliey act best in an alkaline medium, whereas the 

 autolytic enzymes of the lymphatic tflands and most otliei- tissues act best in 

 an acid medium. This leaves little room for doubt that the leucocytes are 

 equipped with their characteristic enzymes when they leave the bone-marrow, 

 and that they are not obtained later in the pancreas or elsewhere. ^Fore re- 

 cently, however, van Calcar (Pfliijier's Archiv., 1012 (148), 2rt~) has revived the 

 idea of the origin of leucocytic enzymes in the digestive ^rlands. 



ooa Peptolytic enzymes appear in the urine after severe superficial burnincr, pre- 

 sumably comins: from the disintegrated cells. (Pfeiffer, INIiinch. med. Wocli , 

 1914 (61), 1329.) 



