RELATION SUPRARENAL GLANDS TO CIRCULATION" 211 



increase followed by a more rapid increase. In the first phase no rela- 

 tion to the general blood-pressure could be perceived. The second stage 

 of 'rapid increase in volume was often of considerable extent and it fre- 

 quently lasted until long after the blood-pressure had fallen to nor- 

 mal. 



A study was then made of the changes in portal blood-pressure and in 

 vena cava pressure in relation to the liver volume changes. The portal 

 pressure showed a preliminary fall followed by a considerable rise that was 

 well sustained. The rise of portal pressure did not coincide with decreased 

 liver volume, as would be the case if it were due to vasoconstriction in 

 the portal system. The increased liver volume was ascribed chiefly to 

 back pressure from the vena cava, since augmented caval pressure ap- 

 peared at the time of the secondary volume reaction and persisted par- 

 tially through it. The fact that the liver volume remained largely aug- 

 mented after the caval pressure had returned to normal, Edmunds ex- 

 plains as due to sequestration of blood in the liver vessels. The published 

 evidence that such is the case does not seem entirely convincing. The 

 general trend of investigations on the relation of epinephrin to venous 

 pressure is to indicate that well-marked systemic reactions, due in turn 

 to local vasomotor effects, can take place without any significant change in 

 venous pressure. 



By direct perfusion experiments Edmunds was able to show that epi- 

 nephrin may cause more or less vasoconstriction in the liver vessels. Sim- 

 ilarly, by the application of epinephrin to isolated sections of portal vein, 

 a reaction to the drug was proved. 



Macleod and Pearce(fr) (1914) have also reported venous outflow 

 studies in the liver. They administered doses of 0.2 to 0.4 mg. of epineph- 

 rin through the pancreatico-duodenal veins of dogs. This caused an imme- 

 diate decrease in the outflow. The result was practically the same, whether 

 the hepatic arteries were ligated or not, a fact which indicates that the ram- 

 ifications of the portal vein in the liver are supplied with vasoconstrictor 

 fibers. These latter results are definitely of only pharmacological signifi- 

 cance, the dosage far transcending physiological Mmits. 



Bainbridge and Trevan (1917) corroborated earlier reports that the 

 administration of epinephrin causes obstruction of the blood flow through 

 the liver and if the infusion is sufficiently prolonged the animal passes 

 into a condition of shock. The partial pressure was recorded from the 

 splenic vein and caval pressure from the iliac. The recording manom- 

 eter was filled with 3.5 per cent sodium citrate solution. The epinephrin 

 caused an augmentation of liver volume and increases flow of lymph from 

 the thoracic duct. Little or no change of caval pressure resulted, under 

 the conditions of their experiments. The authors tentatively concluded 

 that the obstruction was due to "narrowing of the capillary channels by 

 swelling of the liver cells." 



