RELATION SUPRARENAL GLANDS TO CIRCULATION 229 



capacity of the arterial system, a factor which in itself would tend to 

 shunt the blood into the veins. Capps and Matthews (1913) found that 

 small doses of epinephrin do not affect venous pressure, but that larger 

 doses, such as 0.12 mg., cause a rise of from 10 to 80 mm., which coin- 

 cides with marked slowing of the heart. The persistence of the augmented 

 venous pressure coincided with that of the cardiac reaction. Since they 

 obtained a similar effect from faradizing the vagus nerve, they concluded 

 that the rise in venous pressure is to be attributed to the cardiac factor 

 rather than to any venomotor influence of the epinephrin. Bainbridge and 

 Trevan (1917) administered epinephrin after paralyzing the vagus ter- 

 minals in the heart with atropin. Under these conditions they found 

 little or no change in vena cava pressure when epinephrin was injected. 

 They noted, however, a considerable rise of pressure in the portal vein, 

 which they attributed either to a swelling of -the columns of the liver cells 

 narrowing the capillary channels, or a constriction of the radicles of the 

 portal vein. They found that 0.2 mg. of epinephrin caused a rise in the 

 portal pressure of 255 mm. of sodium citrate solution. Kuno also admin- 

 istered epinephrin at a rate which caused accelerated heart-beat and 

 obtained a slight increase in the venous pressure. This he attributed to 

 relative narrowing of the arterial system, forcing more of the blood than 

 normal to the venous side. 



Erlanger and Gasser, in connection with their studies on circulatory 

 failure due to epinephrin, made a few determinations of venous pressure. 

 They used relatively very large doses of the drug administered by vein. 

 In one experiment the jugular pressure changed but little, in two it fell, 

 and in two it rose. 



More recently Connet has investigated somewhat extensively the effects 

 of epinephrin on venous pressure. Her experiments were made on about 

 50 dogs and 25 cats. The dogs were anesthetized with ether and the 

 cats decerebrated. Arterial pressure was recorded with a mercury or a 

 Hiirthle manometer and venous pressures from the superior and inferior 

 cavse were read off from manometers filled wHh sodium citrate solution 

 (2 per cent). Respiration was also graphically recorded. Epinephrin 

 was injected by vein in quantities sufficient always to cause a rise in arte- 

 rial pressure. In order to rule out effects due to changes in respiratory 

 movements curare was administered in some cases. In the curarized, 

 decerebrated cat, such dosages as 0.15 mg. caused an increase in arterial 

 pressure from 34 to 167 mm. of mercury, leaving the pressure in the vena 

 cava unchanged. In one unusual case a fall of venous pressure was noted. 

 In some cases the increase in venous pressure was found to occur to 

 approximately as great extent after as before curarization, hence the 

 author concludes that the respiratory factor plays a minor role. In some 

 cjses the heart rate was increased, in others decreased. Under both 

 conditions augmented venous pressure was seen. In some experiments 



