410 RETROGRESSIVE CHANGES 



have an accumulation of fat in the normal liver merely as a result of 

 increased function, and hence fatty changes may be purely physio- 

 logical in this organ. ■^'^ 



' If the fat accumulates in cells that are structurally normal or 

 nearly so, the fat-droplets fuse together under the pressure of the 

 cytoplasm, and we get the picture of a typical fatty infiltration; in- 

 deed, the only tissues in which we get this typical infiltration are^the 

 liver and the fatty areolar tissue, in both of which the process is pre- 

 sumably physiological in character even if not always physiological 

 in degree. If the cells are much disintegrated through the action of 

 the poison, — e. g., phosphorus, bacterial toxins, etc., — ^the accumulat- 

 ing fat-droplets are not crowded into one large droplet, but He free 

 in the granular debris of the disintegrating cell, constituting the typi- 

 cal appearance of fatty degeneration. Fatty degeneration is usually 

 brought about by poisons, while abnormal fatty infiltration depends 

 usually upon decreased oxidation, due to lack of either oxygen or 

 hemoglobin in the blood. If the anemia is extreme, however, the cells 

 degenerate, and then we find a true fatty degeneration caused by lack 

 of oxygen. "^^ Thus, in an anemic infarct fat accumulates about the 

 periphery of the dead area,^^ probably because fatty acids and glycerol 

 diffuse in slowly from the surrounding parts where circulation still 

 goes on, and are built up into fat by the cell lipase, for in anemic areas 

 the intracellular oxidases cannot destroy these substances as they nor- 

 mally do, because of lack of oxygen. The accumulation of fat in dead 

 areas depends, therefore, on the fact that the constituents of fat can 

 diffuse into the dead tissue, whereas the oxygen, being held in the cor- 

 puscles, cannot enter the anemic area.^^ It is also possible that where 

 fat is set free by autolysis of dead tissue, or when for any cause free 

 fat or lipoid material is present in the vicinity of living cells, it may 

 be phagocyted or in some way infiltrate the cells, causing a fatty meta- 

 morphosis by absorption (Dietrich). 



It is to be supposed that poisons also cause fatty degeneration in 

 a similar way — -by interfering with oxidation. We have much evi- 

 dence that in phosphorus, chloroform, and other poisoning associated 

 with fatty degeneration of the liver, oxidation is impaired."*^ If we 

 imagine for a moment, a cell in which oxidation is checked by any 

 means, we shall have in this cell the lipase and the proteol3^tic 

 enzymes not balanced, as they normally are by the action of the oxi- 

 dases, and hence the processes of cell autolysis and of the accumula- 



" See Coope and Mottram, Jour, of Physiol., 1914 (49), 23; Helly, Beitr. path. 

 Anat., 1914 (60), 1. 



^' Mohr (Zcit. exp. Path., 190G (2), 434), denies that oxidation is decreased in 

 anemia; and in a man with but about half the normal lung area the metabolism 

 was not found iiltored to any extent by Carpenter and Benedict, Amer. Jour. 

 Physiol., 1909 (23), 412. 



« Fisciiler, Cent. f. Path., 1902 (13), 417. 



" See Griesser, Ziegler's Beitr., 1911 (51), 115. 



" See Welsch, Arch. int. de pharm. et therap., 1905 (14), 211. 



