Studies in fat necrosis / by H. Gideon Wells.

  • Harry Gideon Wells
Date:
1903
Catalogue details

Licence: In copyright

Credit: Studies in fat necrosis / by H. Gideon Wells. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    tion of pancreas in a gelatin capsule was placed in contact with the omentum. As this preparation, which he calls “ trypsin,” seems to have been merely dried and pulverized pancreatic tissue, his assumption of a pure tryptic action is quite unwarranted, since the other ferments are not excluded. Dettmer7 first tried the effect of causing pancreatic juice to enter the abdominal cavity, which was accomplished variously by ligating the pancreatic duct, or the ves- sels, or both, by placing pancreas tissue in the abdominal cavity, and by injecting an extract of fresh pancreas. As these caused fat necrosis, he endeavored to find what ferment was responsible, to which end he injected trypsin into still other animals. As trypsin alone did not cause fat necrosis, he concluded that the fat-splitting ferment must be responsible. The trypsin used by Dettmer was quite a different article from that used by Jung, and he describes it as follows: The trypsin used by us (from the firm of Merck in Darmstadt) was studied thoroughly after it was softened in water; it showed no trace of organic structure, but had a more crystal- line appearance; it was designated by the firm as the proteid-splitting substance, in contrast to another preparation, called pancreatin, which contains all active elements of the pancreas. A test of our preparation for a saccharificant action gave a negative result, likewise the test for fat- emulsionizing property. Our preparation was therefore pure trypsin. We obtained with our pure preparation only hemorrhage, no fat necrosis in the Balser-Langerhans sense. It will be observed that no test for lipolytic activity was made. The experiments performed by Dettmer were as follows: (Experiment 1.) Injected into the peritoneal cavity of a cat “ a large quantity of a watery solution of trypsin.” Thirteen days later, the cat having remained well, the abdomen was opened aseptically and nothing abnormal found. About one gram of powdered trypsin was then sprinkled upon the omentum and intestines of this cat (Experiment 3). The animal died in less than twenty-four hours, and autopsy showed great hypersemia and many hemorrhages in the omentum, but the fat itself “ showed no traces of alteration.” There was no evidence of peritonitis. Experiment 2 was a duplicate of Experiment 1, with likewise a totally negative result. This animal then had about 0.5 grams of trypsin placed in the abdomen, after which the wound was closed (Experiment 4). Death occurred seven days later. Autopsy showed no peritonitis; the fat was entirely unaltered, but there were a few small hemorrhages in the omentum. The parts of the intestine that had come in contact with the trypsin were superficially eroded. No histologic examination is mentioned. Dettmer’s conclusions are as follows: These experiments show beyond question that the proteid-splitting ferment, the trypsin, is not able to produce fat necrosis. But, as fresh pancreatic juice is always able to cause fat necro- sis in living fat tissue, there remains nothing more possible except that this action is due to the third ferment contained in pancreatic juice, the fat ferment. Except for the series of experiments just mentioned, the numerous experiments performed by many different investigators have, for the most part, added nothing to the important matter of how the pancreatic juice causes this peculiar form of necrosis, 7 Dissertation, Gottingen, 1895.
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