THE METABOLISM OF THE CARBOHYDRATES 673 



blood may in themselves be responsible for the hyperglycemia (see page 

 332). It can at least be said that when the respiratory disturbances are 

 guarded against, as. by intratracheal insufflation of oxygen, vagal hyper- 

 glycemia is much less marked, if not entirely absent. But this question 

 awaits more thorough investigation. 



The increased glycogenolysis which results from stimulation of the 

 efferent fibers in the splanchnic nerves may depend either on a direct 

 control exercised over the glycogeiiic functions of the hepatic cells, or 

 on the discharge into the blood of some hormone which excites the 

 glycogenolytic process. It must furthermore not be lost sight of that 

 the glycogenolysis may be secondary to local asphyxia! conditions in 

 the liver cells resulting from vasoconstriction. From their anatomic 

 position, the adrenals are to be thought of as the source of the hormone, 

 and evidence that splanchnic hyperglycemia is due to hypersecretion 

 from these glands has seemed to be furnished by the fact that after they 

 are extirpated splanchnic stimulation no longer produces hyperglycemia, 

 neither, indeed, does puncture of the medulla. There is also no doubt 

 that the nervous system, acting by way of the splanchnic nerves, does 

 exercise a control over the discharge of the internal secretion of the 

 adrenal glands and that extracts of the gland, which we must suppose 

 act in the same way as the internal secretion, cause hyperglycemia when 

 injected intravenously (epinephine hyperglycemia and glycosuria). 



But on theoretical grounds alone, certain difficulties immediately pre- 

 sent themselves in accepting this as the mechanism by which the nervous 

 system controls the sugar output of the liver, for if increased sugar 

 formation in the liver is dependent on a discharge of epinephrine, the 

 question may be asked why this secretion should be caused to traverse 

 the entire circulation before reaching the liver. 



There are, besides, certain experimental facts which do not conform 

 with such a view. Thus, after complete severance of the hepatic plexus 

 of nerves, stimulation of the splanchnic nerve does not cause the usual 

 degree of hyperglycemia, whereas electric stimulation of the peripheral 

 end of the cut plexus does cause it. On the one hand, therefore, there 

 is evidence that stimulation of the efferent nerve path above the level of 

 the adrenals has no effect on the sugar production of the liver in the 

 absence of these glands; and on the other, we see that when they are 

 present, stimulation of the nerve supply of the liver is effective, even 

 though the point of stimulation is beyond them. There is but one con- 

 clusion that we may draw namely, that the functional integrity of the 

 efferent nerve-fibers that control the glycogenolytic^ process of the liver 

 depends on the presence of the adrenals, very probably because of the 

 hormone which, the glands secrete into the blood. This conclusion is 



