274 DISTURBANCES OF CIRCULATION 



infarcts in various stages, we get the impression that the diges- 

 tion is accomplished by leucocytes acting on the periphery of the 

 infarct, and not entering the dead area deeply, presumably 

 because of a lack of chemotactic substances in the dead cells. On 

 the other hand, it seems probable that the tissue enzymes them- 

 selves play an important part in the autolysis, for if we implant 

 into animals pieces of tissue in which the enzymes have been 

 destroyed by heating to boiling, it will be found that the cells and 

 their nuclei remain unaifeced for many weeks ; whereas if sterile 

 unheated pieces of tissue in which the enzymes are still active are 

 implanted, they lose their nuclear stain and begin to disintegrate 

 relatively soon, without apparent participation by the leucocytes. 1 

 Ribbert 2 found that in experimentally produced anemic infarcts 

 in the kidney of rabbits the nuclei retain their staining property 

 well for nearly twenty-four hours, becoming then small and 

 deeply stained, undergoing karyorrhexis, and in large part disap- 

 pearing 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 observed 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, gener- 

 ally retain their nuclear stain much longer than cells with 

 more cytoplasm ; this is particularly noticeable in splenic 

 infarcts, where the Malpighian 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 nucleoproteid-splitting 

 enzymes (nuclease, 3 etc.), remains to be determined. It is quite 

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

 of the nucleoproteids of the nucleus by the autolytic enzymes, 

 liberating the nucleic acid, which gives the nuclei the character- 

 istic 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 

 altogether, then, it would seem that the nuclear and cellular 

 alterations that make up the characteristic picture of anemic 

 necrosis are brought about by the intracellular enzymes an 

 autolytic process. The removal of the dead substance, how- 



1 Wells, Jour. Med. Eesearch, 1906 (15), 149. 



2 Virchow's Arch., 1899 (155), 201. 



3 Sachs, Zeit. physiol. Chem., 1905 (46), 337 ; Schittenhelm, ibid., 354. 



