PHAKMACOLOGY AN D TOXICOLOGY OF SUPRARENALS 249 



glycemia and glycosuria which are more marked than would be the case 

 with an intact pancreas. 



On the other side of the question there is evidence that many of these 

 hyperglycemias are more or less independent of epinephrin. Stewart and 

 Rogoff (g) (Jc) have shown that the hyperglycemias of asphyxia and ether 

 anesthesia can occur without any detectable liberation of epinephrin. Ani- 

 mals were employed from which both suprarenals had been removed (rab- 

 bits) or from which one gland had been removed and the nerves to the other 

 cut (cats). A sufficient time was allowed to elapse so that complete recov- 

 ery from the operation might take place and the liver might accumulate 

 glycogen. 



Hyperglycemia could be produced in these animals by asphyxia, ether 

 anesthesia and piqure. ~No epinephrin could be detected in the circulation 

 by methods which are sensitive to one six hundredths of the normal output 

 from intact glands (rabbit's intestine and denervated eye reactions). 



These experiments seem to prove that the suprarenals are not essential 

 for hyperglycogenolysis. Macleod and Pearce(a) had previously concluded 

 that the suprarenal glands play an important part in the control of gly- 

 cogenolysis for it had been found that only when the suprarenals were 

 intact did stimulation of the nerves to the liver cause hyperglycogenolysis. 

 When the suprarenals had been removed such stimulation was without 

 effect. Tying the main suprarenal veins usually produced a similar re- 

 sult. On the other hand these authors found that after complete section 

 of the hepatic plexus, splanchnic stimulation only occasionally produced 

 hyperglycemia although injections of epinephrin when the hepatic plexus 

 was cut caused hyperglycemia. 



In conclusion we may say that epinephrin does not appear to be es- 

 sential to the production of the hyperglycemias of asphyxia, ether and 

 piqure and perhaps other causes. On the other hand epinephrin does 

 stimulate glycogenolysis and may assist in the glycogenolysis produced 

 by other means. (See Keeton and Ross and also Kahn(/).) 



Influence on Body Temperature. Injections of epinephrin which are 

 slowly absorbed may produce a rise in temperature. Thus subcutaneous 

 and intraperitoneal injections are more effective than intravenous injec- 

 tions (Biedl(g)). The cause of the increased temperature is due, at least 

 in part, to the increased heat production (Lusk and Riche; Tompkins, 

 Sturgis and Wearn). 



Sandiford has found that an injection of 0.5 c.c, of 1 :1,000 adrenalin 

 chlorid injected.subcutaneously in the human subject causes an increase 

 in the metabolic rate, the maximum usually occurring within ten to thirty 

 minutes after the injection and lasting from one and one-half to two 

 hours. This increase was usually accompanied by increased pulmonary 

 ventilation. There is a similarity of the metabolic rate curve following 

 epinephrin injection to that found by Lusk in carbohydrate plethora. 



