METABOLISM OF CARBO-HYDRATES GLYCOSURI AS 549 



and yet in the rabbit also the urine remains free from sugar after 

 puncture in the absence of the adrenal glands. In some way or 

 other, then, the adrenals do intervene in the production of puncture 

 glycosuria. The observation, which is easily confirmed, that the 

 injection of adrenalin (or epinephrin) (p. 550) under the skin or into 

 the blood, or into one of the serous sacs, does cause a pronounced 

 increase in the sugar content of the blood, and the appearance of 

 dextrose in the urine, seemed at first to supply the missing link in 

 the chain of evidence. What could be simpler than the assumpt:, n 

 that the splanchnic fibres stimulated in the puncture experiment 

 were fibres going not to the liver, but to the adrenals, which occa-' 

 sioned an outpouring of adrenalin into the blood^and that puncture 

 glycosuria was therefore merely a particular case"of adrenalin glyco- 

 suria ? It is known that excitation of the splanchnic nerves cauces 

 the passage of adrenalin into the blood of the adrenal veins (p. 661). 

 It is known that puncture of the medulla oblongata diminishes the 

 epinephrin content of the adrenal glands. The argument seemed 

 straightforward, and the adrenal hypothesis of puncture glycosr.ria 

 triumphant. As soon, however, as the matter was put to the test 

 of quantitative experiments, the hypothesis began to crumble. It 

 was shown, for example, that during a stimulation of the splanchnic 

 nerves sufficient to cause a decided increase in the dextrose content 

 of the blood, a quantity of adrenalin was given off. to the Adrenal 

 veins, which, when mingled with the rest of the blood on its way 

 to the liver, could not possibly amount to more than one in a hundred 

 million parts of blood, a concentration in which adrenalin, when 

 introduced artificially into the blood-stream, produces no glycosuna 

 whatever. Still more significant is the fact that, after destroying the 

 hepatic plexus, stimulation of the splanchnic nerves causes no in- 

 crease in the blood-sugar in spite of the increased output of adrenalin 

 by the way of the adrenal veins. On the other hand, excitation 

 of the hepatic plexus causes hyperglycsemia (Macleod and Pearce). 

 It is not, then, a direct action on the liver of epinephrin secreted in 

 response to stimulation of splanchnic fibres supplying the adrenal 

 glands which is responsible for the increase in the dextrose content 

 of the blood. The adrenals, however, play some part. For in their 

 absence stimulation of the hepatic plexus is not followed by hyper- 

 glycaemia. But whether this is due to general derangement of the 

 normal carbo-hydrate metabolism in their absence, or to the loss of . 

 some special influence on the liver, without which stimulation of the 

 hepatic plexus is ineffective, is unknown. 



Although several of the operations which lead to temporary 

 glycosuria undoubtedly bring about changes in the hepatic circula- 

 tion, it is as yet impossible to say whether vaso-motor effects con- 

 tribute essentially to the result, or whether it is due entirely to 

 nervous stimulation of the liver-cells, or to withdrawal of such 



