328 DISTURBANCES OF CIRCULATION 



experimentally produced anemic infarcts in the kidneys of rabbits the 

 nuclei retain their staining property well for nearly twenty-four hours, 

 becoming then small and deeply stained, undergoing karj^orrhexis, 

 and in large part disappearing from the convoluted tubules inside of 

 forty-eight hours, although some nuclei may persist in the glomerules 

 for three or more days. In human infarcts, Ribbert believes, the 

 process goes on faster, for he has osberved here a loss of nuclei within 

 twenty-four hours. These nuclear changes undoubtedly depend upon 

 autolysis, but it is probable that the enzymes concerned reside in the 

 cytoplasm rather than in the nucleus, for I have observed that cells 

 of lymphoid type, with practically no cytoplasm, generally retain 

 their nuclear stain much longer than cells with more cytoplasm; this 

 is particularly noticeable in splenic infarcts, where the ]\Ialpighian 

 corpuscles retain their staining affinities much longer than the pulp 

 elements. Whether the destruction of the nuclei is accomplished 

 by the ordinary intracellular proteases, or by special nucleoprotein- 

 splitting enzymes (nuclease, ^^ etc.), remains to be determined. It is 

 quite possible, however, that the first changes consist of a splitting 

 of the nucleoproteins of the nucleus by the autolytic enzymes, liber- 

 ating the nucleic acid, which gives the nuclei the characteristic intense 

 staining with basic dyes (pycnosis) observed in areas of early anemic 

 necrosis. The nucleic acid may then be further decomposed by the 

 nuclease or similar enzymes. Taken all together, then, it would seem 

 that the nuclear and cellular alterations that make up the character- 

 istic picture of anemic necrosis are brought about by the intracellular 

 enzymes — 'an autolytic process. The removal of the dead substance, 

 however, seems to be accomplished rather by the invading leucocytes, 

 through heterolysis. The relatively small part taken by the intracel- 

 lular enzymes may possibly be due to the seeping through them of alka- 

 line blood-plasma, for autolytic enzymes are not active in an alkaline 

 medium; the leucocytic enzymes, however, act best in an alkaline 

 medium. 2^ 



About the periphery of infarcts is usually observed more or less fat 

 deposition (Fischler),^" particularly in the endothelial cells (Ribbert). 

 This is not peculiar to infarcts, however, for Sata^' found a similar 

 peripheral fatty metamorphosis common to all necrotic areas. The 

 basis of this is possibly the persistence of the cell lipase, wliich syn- 

 thesizes fatty acid and glycerol diffusing into the necrotic area with 

 the plasma, unchecked by normal oxidative destruction of these 

 substances. (See "Fatty Degeneration," Chap, xvi.) 



Hemorrhagic infarcts offer in addition to the changes conunon 

 to anemic infarcts, the alterations occurring in' the blood-corpuscles. 



"» Sachs, Zoit physiol. Chcm., 1905' (4C), '337; Schittonhclni, ibid., 354.' 

 ^^ More fully discussed by Wells,-" loc. cit., and under necrosis, Chap. xv. 

 30 Cent. f. Path., 1«)()'2 (13), 417. 

 " Ziegler's lieitr., 1900 (28), 461. 



