132 MEDULLA 



a conversion of pre-existent glycogen into glucose has been 

 advanced by Cori and Cori. 128 These authors showed that 

 the mobilization of all the glycogen present in the liver could 

 only account for part of the glucose which appears in the cir- 

 culation after an injection of epinephrine. In fasting rats, 

 these authors found that epinephrine caused a decrease in the 

 glycogen content of the muscles with a concurrent increase in 

 the glycogen store of the liver. Cori and Cori considered the 

 changes induced by epinephrine as consisting of a breakdown 

 of glycogen in the muscles to lactic acid, a resynthesis of this 

 lactic acid in the liver to glycogen, and a breakdown of the 

 liver glycogen to the glucose which appeared in the blood. 



Corkill and Marks 129 demonstrated that in eviscerated cats, 

 epinephrine causes a discharge of epinephrine from the resting 

 muscles. None of this glycogen appears in the form of glucose 

 and only a part of it as lactic acid. The remaining carbohy- 

 drate may be in the same form as the so-called "lost carbo- 

 hydrate" which disappears after the injection of insulin. Its 

 appearance may be due to the action of the epinephrine liber- 

 ated by insulin. MacCleod, 419 however, has cast doubt on 

 the existence of this "lost carbohydrate." 



When the glycogen store of the liver is reduced by injections 

 of phlorizin, hypoglycemia follows epinephrine injections. 

 This depression of the blood sugar level is attributed by 

 LaBarre and Houssa 371 to the stimulation of the secretion of 

 insulin by the epinephrine. 



The failure of piqure after section of the splanchnic nerves 

 to induce hyperglycemia is explained by the lack of epinephrine 

 secretion in the denervated glands. Stewart and Rogoff 588 

 and MacLeod, 419 however, have concluded that the presence 

 of the adrenals is not necessary for the development of the 

 hyperglycemia which follows decerebration or piqure. The 

 impulses transmitted along the sympathetic pathway from the 

 diabetogenic center in the pons must therefore act independ- 

 ently of the adrenal glands and influence the glycogenic func- 



