722 HENRY G. BARBOUR 



Salt Glycosuria. This phenomenon, which has been investigated 

 chiefly in rabbits, bears an undoubted relation to salt fever. It was dis- 

 covered in 1871 by Bock and Hoffmann as the result of injecting into 

 the arterial circulation of rabbits large amounts of 1 per cent sodium 

 chlorid. Others have added to the list of glycosuria-producing salts the 

 acetate, bicarbonate, phosphate, succinate, valerianate and sulphate of 

 sodium. Kleiner and Meltzer(&) have shown that the last mentioned pro- 

 duces no hyperglycemia, thus differing from magnesium sulphate (see 

 below). 



A number of authors have considered the possibility that salt acting 

 through the central nervous system may exert a stimulating influence upon 

 the adrenal glands. This would accord with Freund's parallelism between 

 the glycosurias and fevers caused respectively by salt, sugar and epineph- 

 rin. Furthermore, Waterman and Smit found an increased epinephrin 

 content in "the blood in salt glycosuria, while Stewart and Rogoff(a) have 

 recently shown that concentrated sodium carbonate solutions increase the 

 epinephrin output from the adrenals. Mobilization of glycogen by salt 

 through the agency of these glands would thus seem to be strongly 

 suggested. 



However, MacGuigan's demonstration that epinephrectomy in cats is 

 without influence upon salt glycosuria (although in dogs the operation 

 does make the glycosuria more difficult of accomplishment) seems to 

 exclude the adrenals as the prime causative factor. 



Fischer (a) found that the intravenous injection of sodium chlorid (one- 

 sixth molecular_or stronger) causes glycosuria in rabbits after a certain 

 latent period. Weaker solutions exert less effect or none at all. The 

 addition of calcium chlorid prevents or puts an end to the appearance of 

 sugar; the latter reappears, however, after returning to pure sodium 

 chlorid. Fischer was inclined to exclude osmosis as a factor because urea, 

 glycerin and alcohol all failed to produce glycosuria. Since salt injec- 

 tions into arteries leading directly to the brain caused quicker and more 

 profound results the theory of a central action was favored. 



The blood sugar in salt glycosuria was investigated by Underbill and 

 Closson, who found it diminished. Underbill and Kleiner (6) were able to 

 inhibit the hypoglycemia and glycosuria as well as the accompanying 

 polyuria by calcium chlorid whence they concluded that the latter restores 

 the retaining power of the kidney for glucose which sodium chlorid appar- 

 ently impairs. The calcium injection even made the kidneys unusually 

 impermeable to injected glucose which affords a counterpart to Pavy 

 and Godden's experiment in which sodium chlorid was shown to reduce 

 the tolerance of rabbits towards injected sugar. Salt glycosuria was there- 

 fore attributed by Underbill and his co-workers to increased renal perme- 

 ability; dyspnea was invoked as an additional factor, for in the case of 

 arterial injections hyperglycemia and glycosuria without polyuria were 



