n EXTEKNAL DIGESTIVE SECKETIONS 99 



that the function of the gland appeared not to be indispensable in 

 the various processes of metabolism. 



Nor did glycosuria appear in other experiments (on dogs, cats, 

 and rabbits) in which destruction of the pancreas was attempted 

 in situ by ligation and section of the ducts, or their injection with 

 extraneous substances, such as oil, paraffin, acids, etc. (Cl. Bernard, 

 Schiff, Pawlow, Arnozan, and Vaillard). 



In 1889 von Mering and Minkowski successfully accomplished 

 the total excision of the pancreas in dogs, and stated that 

 immediately after the operation there appeared regularly, along 

 with grave disturbances of alimentary absorption, an intense 

 glycosuria which lasted until the death of the animal, 2-3 weeks 

 later. The complex of symptoms was very like that of severe 

 cases of human diabetes (wasting diabetes}, so much so that it 

 was known by the name of experimental diabetes. 



The results of von Mering and Minkowski were at once 

 confirmed by many authorities (Hedon, Lepine, Capparelli, etc.). 

 Since this glycosuria was evidently not due to impeded flow of 

 pancreatic juice into the intestine (as in the case of the permanent 

 fistula of Wirsung's duct), it was easy to deduce that it depended 

 not on the defective action of the secretion in the intestine, but on 

 the suppression of some other function exerted by the pancreas. 

 This idea, however, was and still is combated by some authors on 

 the strength of the following experiments. 



De Dominicis, who excised the pancreas in dogs, simultaneously 

 with von Mering and Minkowski, sustained emphatically that the 

 glycosuria was not a constant phenomenon, and not in any case 

 determined by the suppression of an internal pancreatic secretion. 

 Glycosuria and all the other phenomena by which it is usually 

 accompanied (pollakiuria, polyuria, polyphagia, azoturia, phospha- 

 turia, etc.) depend, according to De Dominicis, upon a reabsorption 

 of toxines formed by the putrefaction of alimentary substances 

 that are not digested owing to lack of pancreatic juice. He 

 observed that injection of faecal extract from depancreatised dogs 

 produces slight glycosuria (1894), while injection of the duodenal 

 contents of depancreatised dogs produces an intense and persistent 

 glycosuria (1908). 



Pflliger (1905) long refused to admit that the glycosuria conse- 

 quent on excision of the pancreas was due to suppression of a true 

 internal function of this gland. In his opinion the operative act 

 excites the nerve plexuses which traverse or have their terminations 

 near the pancreas, and which reflexly affect the centres which he 

 terms didbetogenic, leading to increased formation of glucose on 

 the part of the liver. This theory of Pfltiger, already brought 

 forward in 1892 by the brothers Cavazzani, was contradicted by 

 the experimental results of Lustig, Kaufmann, Marassini, Zamboni, 

 who, on more or less completely excising the solar plexus, or 



