v INTEENAL EESTITUTIVE SECRETIONS 307 



hepatic diastase), and that the direct or indirect excitation of these 

 produces the exaggerated glycogenesis and consequent glycosuria 

 observed as the effect of various nerve lesions. 



In support of this hypothesis A. and E. Cavazzani brought 

 forward experimental results which appear to us of considerable 

 value. In 1892 they found that stimulation of the caeliac plexus 

 with an induced current, lasting for a few minutes, augments the 

 sugar content of the blood flowing from the liver. In 1894 it 

 occurred to them to use this means of increasing hepatic 

 glycogenesis, both in living and in recently killed animals, not 

 merely to confirm the fact that increase of sugar in the liver 

 coincides with a diminution of glycogen, but also to see if the 

 phenomenon changes in correspondence with the activity or arrest 

 of the circulation in the liver. They extirpated a hepatic lobe 

 from live and from recently killed dogs, and then stimulated the 

 caeliac plexus for about 15 



minutes. A second lobe A B 



was then excised, after 

 which they estimated the 

 glucose and glycogen in 

 both lobes, after weighing 

 and boiling them. The 

 results of their experiments 

 are briefly as follows: In 



living animals Stimulation Flo . 97 ._ He patic cells of dog after fasting 36 hours 



Of the Caeliac pleXUS pro- <> j and U hours after an abundant meal (B). 



, r . (Heidenham.) In A the cells are small and finely 



duceS a marked increase OI granular; at B they are much magnified by the 



1 *-V, I;,T J accumulation of glycogen, a hyaline substance that 



glUCOSe in the liver and a obscures the granulations of the cytoplasm. 



comparatively greater 



diminution of glycogen, because part of the sugar is carried away 

 as fast as it is formed by the blood current. In freshly killed 

 animals in which the circulation is at a standstill, the same 

 stimulation still produces increased glycogenesis, and the corre- 

 spondence between the glucose formed and the glycogen that 

 disappears is absolute or nearly so. From this we may conclude : 

 (a) that stimulation of the nerve fibres which run from the 

 caeliac plexus to the liver increases the hepatic glycogenesis ; 

 (6) that the sugar formed comes from conversion of the glycogen ; 

 (c) that this conversion is up to a certain point independent 

 of the external circulatory conditions, so that it is improbable 

 that the influence of the nervous system on hepatic glycogenesis 

 consists in a simple vasomotor action leading to increased irrigation 

 of the liver with blood. 



E. Cavazzani further demonstrated that the glycogenesis pro- 

 moted by excitation of the caeliac plexus is accompanied by cyto- 

 logical changes in the hepatic cells, similar to those which Afanasiew 

 and others detected in the liver of fed and fasting animals (Fig. 97). 



