346 THE ADRENAL, GENERAL MOTOR, AND VAGAL SYSTEMS. 



in the afferent venous channels, since it is very improbable 

 that any oxidizing substance, so precious in all physiological 

 functions (at least so it appears to us), should be wasted in 

 vessels ultimately ending, via the hepatic veins, in the inferior 

 vena cava. Hence, whether it involved a preliminary forma- 

 tion of an ammonic carbamate or proceed to immediate syn- 

 thesis, it appears as if the terminal reaction ending in the forma- 

 tion of urea occurred in the efferent venous hepatic channels. 



The salient point of this series of reactions is the fact 

 that, contrary to the general belief, they all occur, not in the 

 hepatic cells, but in the blood-stream of the lobular capillaries. 

 The following facts show this to be the case: It is clear that, 

 if urea is formed in transit through the vessels of the organ, 

 it should appear as soon as, or at least soon after, its causative 

 agencies are introduced in the portal system. We will recall 

 the quotation from Professor Foster's text, in which he says: 

 "The introduction of even a small quantity of proteid mate- 

 rial into the alimentary canal at once increases the urea in 

 the urine, and in the curve of the . discharge of urea in the 

 twenty-four hours each meal is followed by a conspicuous rise, 

 etc." When we consider that the entire circulatory circuit 

 occupies but twenty-six seconds, the cause of the rapid appear- 

 ance of urea heretofore unexplained becomes apparent. 



When the role of the oxidizing substance in the produc- 

 tion of uric* acid from the alloxuric bases was analyzed in the 

 third chapter, uric acid was considered as the end-product of 

 a series of reactions in which, according to modern views, these 

 toxic nuclein derivatives were converted into benign ones. All 

 nitrogenous products being transferred to the portal system, 

 it now seems clear that normally the reaction must occur in 

 the intercellular capillaries of the hepatic lobules, and that it 

 is when this oxidation process in the liver is inadequate that 

 the so-called "uric-acid diathesis" symptoms occur. As uric 

 acid leaves the organism, as does urea, by the urine, it is 

 evident that we are again dealing with a function totally dis- 

 connected from the hepatic cell per se. Again, we have re- 

 peatedly seen, in the preceding chapters, that the elimination 

 of phosphoric acid was increased by the administration of 

 suprarenal, pituitary, and other organic extracts and by various 



