GLYCOSURIAS. 3S1 



which occur after other lesions of the nervous system, belong to the 

 above group of glycosurias. The glycosuria produced on poisoning 

 with carbon monoxide, ether, chloroform, curare, strychnine, morphine, 

 piperidine, etc., also belongs to this group. How these 'glycosuria^ 

 are brought about is not known with certainty, and the conditions 

 become complicated because in most cases the appearance of the gly- 

 cosuria is connected with an insufficient supply of oxygen. UNDERBILL 

 has shown for the piperidine-glycosuria and PENZOLDT and FLEISCHER 

 and SAUER l for the curare-glycosuria that one can prevent the appear- 

 ance of the glycosuria (on poisoning with piperidine) a,nd the hyper- 

 glycsemia as well by supplying oxygen. MACLEOD 2 has also shown that 

 the irritation of the central end of the cut vagus, or irritation of the spinal 

 marrow, produces glycosuria and hyperglycaBmia only with simultaneous 

 dyspnoea; with sufficient oxygen supply the glycosuria remains absent. 

 This does not conflict with the ordinary assumption that in this group 

 of glycosurias an increased formation of sugar occurs from the gly- 

 cogen. The investigations of BANG, LJUNGDAHL and BoHM, 3 in which 

 the extent of enzymotic decomposition of glycogen in the liver was 

 determined, also indicate positively that in the piqure as well as in the 

 asphyxia of strychnine and morphine poisoning an increased decomposi- 

 tion of glycogen takes place. 



The material from which the sugar is formed is glycogen in most 

 cases. That the glycosuria produced after piqure is due to an increased 

 transformation of the glycogen follows from the fact that no glycosuria 

 appears, under the above-mentioned circumstances, when the liver has 

 been previously made free from glycogen by starvation or other means. 

 In other cases, as in carbon-monoxide poisoning, the origin of the sugar 

 is less clear. In the last-mentioned case a sugar formation from pro- 

 teins has indeed been accepted, as this glycosuria appears only in 

 those cases when the poisoned animal has a sufficient quantity of protein 

 at its disposal (STRAUB and RosENSTEiN 4 ). Protein starvation with a 

 simultaneously abundant supply of carbohydrates causes this glyco- 

 suria to disappear. In the glycosuria produced by irritation of the 

 vagus, which as above remarked, according to MACLEOD only appears 

 with insufficient supply of oxygen, the hyperglycsemia (in rabbits) 



1 Underbill, Journ. of biol. Chem., 1; Penzoldt and Fleischer, Virchow's Arch., 87; 

 Sauer, Pfluger's Arch., 49, 425, 426. 



2 Macleod, Amer. Journ. of Physiol., 19, with Briggs, Cleveland Med. Journ., 1907. 



3 Hofmeister's Beitrage, 9 and 10. 



4 See Dock, Pfluger's Arch., 5; Bock and Hoffmann, Exp. Studien uber Diabetes 

 (Berlin, 1874) ; Cb Bernard, Lemons sur le diabete (Paris) ; T. Araki, Zeitschr. f . physiol. 

 Chem., 15, 351; Straub, Arch. f. exp. Path. u. Pharm., 38; Rosenstein, ibid., 40; 

 Pfluger, Pfluger's Arch., %. 



