Tin mi TABOl [8M OF Tin: CAftBOfiYDBAtES 



blood may in themselves be responsible for the hyperglycemia see pi 

 332). 1 1 can .-it leasl be said thai when the respiratory disturbances are 

 guarded against, as by intratracheal insufflation of oxygen, vagal hyp 

 glycemia is much less marked, if nol entirely absent. But ihis question 

 awaits more thorough investigation. 



Tlio increased glycogenolysis which results from stimulation of the 

 efferent filters in the splanchnic oerves maj depend either on a direcl 

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

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

 glycogenolytic process. It must furthermore ool be lost sight of thai 



the glycogenolysis may be s Ldary to local asphyxia] conditions in 



the liver cells resulting from vasoconstriction. Prom their anatomic 

 Position, the adrenals are to be thought of as the source of the hormo 

 and evidence that splanchnic hyperglycemia is due to hyp, tion 



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 eland, which we must BUppose 

 aet in the same May as the internal secretion, cause hyperglycemia when 

 injected intravenously (epinephine hyperglycemia and glycosuria . 



Bu1 on theoretical grounds alone, certain difficulties immediately pre- 

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



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



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



question may be asked why this Secretion should be caused to trav< 



the entire circulation before reaching the liver. 



There are, besides, certain experimental facts which do nut conform 

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

 of aerves, stimulation of the splanchnic nerve docs not cause the usual 

 degree of hyperglycemia, whereas electric stimulation of the peripheral 



end of the cut plexus docs cause it. (Mi the one hand, therefore, t! 



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 con- 



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



efferent nerve libers 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 



