524 TEXT-BOOK OF PHYSIOLOGY 



the medulla, which are then stimulated to increased activity. As to 

 whether the puncture of the medulla excites the activities of vaso-motor 

 or of secretor cells there is much obscurity. Whatever the nature of the 

 impulses thus generated, the further question arises, as to the pathway 

 by which the nerve impulses pass, whether by way of the vagi or by way of 

 the spinal cord and the splanchnic nerves, and the hepatic plexus formed in 

 part by the post-ganglionic fibers from the cells of the semilunar ganglion. 

 That it is not, by way of the vagi, is shown by the fact that division 

 of these nerves does not interfere with the development of glycosuria, 

 nor prevent it, after it is once established. That the pathway is down 

 the spinal cord and subsequently through the splanchnics, is indicated 

 by the fact that a transverse division of the spinal cord above the level 

 of origin of these nerves, as well as a division of the splanchnics, prevents 

 the development of the glycosuria that otherwise would follow punc- 

 ture of the medulla. It must be remembered, however, that a transverse 

 division of the spinal cord in itself frequently gives rise to a temporary 

 glycosuria. Though the results of experimentation are not in all respects 

 in agreement, yet there is evidence that the pathway is continued through the 

 splanchnic nerve particularly on the left side as far as the semilunar ganglion 

 and thence through the hepatic plexus. 



Though stimulation of the left splanchnic nerve is usually followed by 

 glycosuria, the question arises whether this effect is due to direct nerve stimu- 

 lation of the liver cells, thus increasing glycogenesis or glycogenolysis, or 

 whether it is due to an increased amount of adrenal secretion in the blood, 

 which is discharged into it during the time of splanchnic stimulation. The 

 following facts will serve to elucidate the relationship between these organs. 



It is well known that the subcutaneous injection of one milligram of 

 adrenalin chlorid per 1000 grams of body- weight, will give rise to hyper- 

 glycemia and glycosuria. Stimulation of the left splanchnic nerve just where 

 it sends branches to the adrenal gland, gives rise to an increased secretion 

 and its discharge into the blood as can be shown in many ways. From these 

 facts the deduction is made that the glycosuria is the result of an increase in 

 the normal percentage of adrenalin in the blood and this latter fact, is due 

 to splanchnic stimulation. This supposition is strengthened by the further 

 fact that after removal of the adrenal glands, neither puncture of the medulla 

 nor stimulation of the splanchnics gives rise to glycosuria except in rare 

 instances. 



It is not to be inferred, however, that the mere presence of adrenalin in 

 the blood is the cause of the increased activity of the liver cells and hence of 

 the hyperglycemia and glycosuria, for if the hepatic plexus be divided, thus 

 preventing nerve impulses from reaching the liver, the increased per- 

 centage of adrenalin in the blood fails to cause glycosuria. That another 

 factor is present is evident from the following: Stimulation of the hepatic 

 plexus, which presumably 'influences the production of sugar, always gives 

 rise to glycosuria when the adrenal glands are intact but never after their 

 removal. Hence the assumption is made that the production of sugar by 

 the liver glycogenolysis is under the control of the central nerve system 

 and by the route detailed in foregoing paragraphs, but only when a suffi- 

 cient amount of adrenalin is present in the blood. The r61e assigned to 

 the adrenalin is a heightening of the irritability of the terminal branches of 



