248 FRANK A. HARTMAN 



effect of the epinephrin is greater when large amounts of glycogen are 

 stored. If ifhere is but a scanty glycogen storage larger doses of epinephrin 

 are required to bring about a given result. 



Ritzmann has shown that intravenous are more effective than subcu- 

 taneous injections. This is true when the epinephrin is infused over a 

 period of time. As much as 80 per cent of the epinephrin injected sub- 

 cutaneously appears to be without effect judging from the fact that it re- 

 quired five times as much epinephrin subeutaneously to cause the ex- 

 cretion of the same amount of sugar as that obtained from intravenous 

 administration. Much of the epinephrin must have been destroyed before 

 it reached the circulation. 



Small doses of epinephrin may cause no measurable depreciation in 

 the amount of glycogen in the liver in well nourished animals. Only 

 when toxic doses are employed can these changes be brought about (Drum- 

 mond and Paton). Glycogen may disappear from both the muscles and 

 liver if a large amount of epinephrin is used (Agadschanianz). Pollak 

 found that levulose-glycogen was more resistant to epinephrin than was glu- 

 cose-glycogen. Pentose mobilization is also resistant to epinephrin. Coseii- 

 tino has been unable to produce pentosuria from injection of the latter. 



Phocas has been able to obtain epinephrin glycosuria in rabbits de- 

 prived of their glycogen by fasting. He suggests as an explanation of 

 this, the action of hepatic diastases upon substances other than glycogen 

 (lipoids, glycoproteins) resulting in the formation of glucose. It is 

 assumed that epinephrin increases the hepatic diastases. As an indication 

 that the glucose came from a larger molecule he found a notable increase 

 in the excretion of urea and phosphates after epinephrin injection. How- 

 ever these would not necessarily be residues of the molecules from which 

 the glucose might be formed. 



Blum (a) has suggested that the glycosuria resulting from Bernard's 

 puncture is due to a release of epinephrin through stimulation of the 

 splanchnic nerves. Mayer (>) failed to obtain glycosuria from diabetic 

 puncture after the suprarenals were removed. In addition Waterman and 

 Smit have found an increase in the output of epinephrin after puncture 

 of the fourth ventricle. 



Kalm(/) has concluded that through the action of the splanchnic nerve 

 sugar puncture makes the liver cells more sensitive to epinephrin action 

 arid also stimulates epinephrin secretion. Due to an increased sensitive- 

 ness of the glycogenolytic mechanism of the liver sugar may be released 

 even in the absence of the suprarenal s, although the sugar release is much 

 more marked in their presence. 



The pancreas opposes the action of epinephrin in the mobilization of 

 sugar as shown by Achard, Ribot and Binet and also by the following 

 experiments. If the pancreas has been removed in dogs either puncture 

 of the fourth ventricle or injection of epinephrin produces both hyper- 



