DISTURBANCES OF PAXCREATIC METABOLISM 689 



In a series of experiments these authors were able to demonstrate, by 

 previous injections of trypsin, a degree of acquired immunity in the 

 animals. Experimental pancreatitis produced in these animals by injec- 

 tion of oil into the Wirsungian duct caused pancreatic necrosis and atro- 

 phy, but not death nor toxic collapse. Von Bergmann and Gulecke speci- 

 fically state that they do not understand death in pancreatic disease as due 

 either to the trypsin or steapsin liberated ; they attributed the fatal out- 

 come to a toxic protein formed in the autolyzing pancreatic tissue; in 

 their experiments they utilized trypsin as an agent with which to im- 

 munize against this unknown toxin. 



The researches of Lattes have added much to our conception of the 

 formation of this toxic product, The intraperitoneal injection of pan- 

 creatic juice in which the trypsin was inactivated, though the steapsin was 

 active, failed to produce an effect in dogs. The injection however of acti- 

 vated fluid from a pancreatic fistula caused toxic death in a few hours with 

 symptoms of collapse, peritonitis, hemorrhage and acute nephritis. The 

 same phenomena were seen in all experiments, independent of whether the 

 lipolytic ferment of the injected fluid was active or not. 



Intraperitoneal fistula caused fat necrosis but no dangerous symptoms 

 in the animal, unless duodenal juice was injected as an activating sub- 

 stance. In the latter case death took place within nine hours. Lattes con- 

 cludes that the fatal intoxication is due to increased potency of the proteo- 

 lytic power of the pancreas when activated by intestinal juice. The 

 toxin thus produced, while thermolabilo, is more stable than the proteo- 

 lytic ferment, and can in this way be separated from it. Pure autolyzed 

 pancreatic tissue, injected, was ineffectual, as was also the inactivated 

 pancreatic juice. Both injected at once caused rapid death with fat 

 necrosis. 



Death in trauma or rupture of the pancreas is due to activation of the 

 liberated pancreatic secretion by the necrosing tissue cells. Ligation of 

 the vessels of the gland after experimental traumatism to the gland re 

 suits in acute pancreatic necrosis often with death in animals (Lattes). 

 Levin places emphasis on the interference with circulation as being an 

 essential factor. Lacking this, even severe crushing or ligaturing does not 

 necessarily produce acute necrosis or a fatal result. 



Since 1916, the American literature has contained several important 

 contributions tending more accurately to identify the toxic protein element 

 in pancreatic necrosis. In that year Whipple announced the isolation from 

 the pancreas of an animal in which an experimental hemorrhagic necrosis 

 had been produced, of a toxic proteose which he considered an active agent 

 in the production of the symptoms. This proteose he regarded as analo- 

 gous to the proteose he had demonstrated in acute intestinal obstruction 

 and in acute peritonitis. Petersen, Jobling and Eggstein have shown 

 that in experimental acute pancreatitis the incoagulable nitrogen of the 



