PHARMACOLOGY AND TOXICOLOGY OF STJPRARENALS 247 



jections of suprarenal extract. This was observed in animals deprived 

 of carbohydrates as well as those which were starving. Very soon after 

 this, Herter found that the injection of epinephrin into the peritoneal 

 cavity produced marked glycosuria. He believed this was due to action 

 on the pancreas because painting the latter produced glycosuria while 

 the injection of epinephrin into the liver had less effect. 



Paton(a) believed that this condition was a true diabetes for it occurred 

 after the stored carbohydrates had been removed from the body by phlorid- 

 zin. Moreover, he found that there were disturbances in the distribution of 

 nitrogen in the urine similar to those occurring in diabetes. On the 

 other hand Underhill and Closson were unable to find any alteration in 

 the distribution of nitrogen from subcutaneous injections of epinephrin. 



Paton(&) has used ducks and geese in an attempt to show whether the 

 pancreas is involved in epinephrin glycosuria. V. Mering and Minkowski 

 had already proven that removal of the pancreas in these birds did not 

 cause diabetes. Paton found that he could produce glycosuria by the 

 injection of epinephrin after removal of the pancreas. He concluded 

 that epinephrin does not act through the pancreas. 



It has been suggested by Underhill and Closson that the mechanism 

 of epinephrin glycosuria is of nervous origin, acting through the sympa- 

 thetic system. This action is due to a stimulation of the organs storing 

 glycogen causing a release or preventing storage or both, hyperglycemia 

 and glycosuria resulting. Achard, Eibot and Binet have performed ex- 

 periments on dogs which support the idea that epinephrin prevents the 

 storage of sugar. They found that the simultaneous injections of sugar 

 and epinephrin produced a greater hyperglycemia than the sum of the 

 increases obtained from the injection of like quantities of the two sub- 

 stances at different times. The duration of the hyperglycemia was also 

 prolonged. Fresh pancreas extract added to the glucose-epinephrin mix- 

 ture reduced the hyperglycemia. 



Epinephrin glycosuria is due to hyperglycemia great enough to cause 

 sugar overflow through the kidney. At first it seems that excess sugar 

 escapes from the kidney more easily, while with succeeding doses the escape 

 becomes more difficult and may not occur at all. This does not appear to 

 be due to a decrease in the amount of sugar in the blood but more to an 

 increased power of the kidney to block the exit of sugar (Pollak(a)). 

 When glycosuria appears it is said to last only as long as there is epinephrin 

 in the blood (Ritzmann). A continuous injection of epinephrin diluted 

 1 :2 million may not produce glycosuria when injected at the rate of 1 c.c. 

 per minute, but a velocity of 3 to 4 c.c. per minute may be sufficient to do 

 so. There is a long latent period due perhaps to the time required for 

 the transformation of the glycogen to sugar. The amount of sugar released 

 is said to be in proportion to the amount of epinephrin available per unit 

 of time, this being the case only within a certain range. However, the 



