METABOLISM OF CARBO-HYDRATESGLYCOSURIAS 541 



stimulation of the splanchnic nerves causes no increase 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 hyper glycaemia (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 hyperglycsemia. 

 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 

 stimulation or control (see also p. 502). There is some evidence 

 that excitation of the uncut great splanchnic nerve (on the left side) 

 in dogs may cause hyperglycaemia, diuresis, and glycosuria, even 

 under conditions in which as far as possible circulatory effects are 

 eliminated. Contrariwise, when in the puncture experiment on an 

 unnarcotized animal the small instrument does not wound the 

 medulla oblongata in the right place, a rise of blood-pressure due 

 to excitation of the vaso-motor centre may occur without any 

 glycosuria. But absolute proof of the existence of glycogenolytic 

 nerve fibres going to the liver that is, fibres whose stimulation 

 accelerates the hydrolysis of glycogen into dextrose (Macleod) has 

 not yet been brought forward. 



f Adrenalin Glycosuria.W-In adrenalin glycosuria the sugar-content 

 6i the blood is increased.) /Subcutaneous injection of adrenalin 

 chloride causes a mild, intravenous injection a greater glycosuria, 

 and intraperitoneal injection the greatest glycosuria of allj(Herter). 

 The best evidence is that the glycosuria is produced by some action 

 on the liver, possibly through the excitation of sympathetic fibres 

 controlling the production of dextrose from glycogen (Underbill and 

 Closson), or by a direct effect on the hepatic cells, which hastens the 

 normal transformation of glycogen into dextrose, or hinders the 

 normal transformation of dextrose into glycogen. It has been 

 stated that in the isolated surviving liver of the frog adrenalin causes 

 the glycogen to be rapidly converted into dextrose. While this 

 confirms the view that experimental adrenalin glycosuria is due to 

 an action on the liver which increases the sugar-content of the blood, 

 it does not necessarily show that the action is exerted directly on 

 the hepatic cells without the intervention of nerve fibres. For the 



