140 G. K STEWART 



nephrin stole under anesthesia, etc., is situated in the bulb close to the vaso- 

 motor centers, and that depletion does not occur when the cord is divided 

 below this level, under the influence of conditions which would other- 

 wise have caused it. But observations on the store cannot be directly trans- 

 ferred to the liberation of epinephrin from the suprarenals. One of 

 the best illustrations of this is the fact that, as shown by Elliott, it is 

 difficult to produce by stimulation of the splanchnic any detectable change 

 in the store of epinephrin, while the liberation is markedly increased. 

 The simplest explanation would seem to be that the splanchnic also con- 

 tains fibers which increase the rate of formation of epinephrin in the gland, 

 as suggested by Tscheboksaroff(#). It is not inconsistent with this that 

 after section of the splanchnic, and indeed, as far as possible, of all the 

 nerves going to the suprarenal, a depletion in the store is entirely made 

 good in a day or two. The chromaphil cells may very well have the power 

 of accumulating epinephrin in the absence of innervation up to a certain 

 maximum, and if they are losing none, as after section of the nerves, a 

 considerable deficiency may be made up in 24 or 48 hours. But under 

 the rapid mobilization which occurs when the secretory nerves are stimu- 

 lated, it might be expected that the replenishment of the store should 

 also bo accelerated. With very prolonged stimulation of the splanchnic 

 (9 hours), with short periods of excitation alternating with longer rest 

 periods so that each stimulation is effective, a distinct depletion was found 

 after 300 stimulations by Stewart and Rogoff(c) (1916). They concluded 

 that an amount of epinephrin approximately equal to the initial load 

 (0.20 mgm.) must have been formed in the gland whose splanchnic was 

 stimulated during the time the experiment lasted. 



Concerning the possible afferent paths through which the epinephrin 

 output can be affected, little or nothing is known. Richards and Wood(fr), 

 working with rabbits and testing the suprarenal vein blood collected from 

 a cava pocket on cat's intestine strips, came to the conclusion that stimu- 

 lation of the depressor caused diminution of the rate of liberation of 

 epinephrin. Incidentally they observed that stimulation of sensory nerves 

 (central end of the median) did not increase the output. Tscheboksaroff (a) 

 from the increase of blood pressure produced in a dog by the injection of 

 suprarenal vein blood from another dog convinced himself that "the 

 increase of blood-pressure caused by stimulation of a sensory nerve (sci- 

 atic) has no effect upon the quantity of secreted adrenalin." 



Cannon and Hoskins withdrew blood from the inferior cava by a fine 

 catheter passed up through the femoral vein to above the level of the 

 suprarenals (in cats), and tested the blood on rabbit's intestine segments. 

 They concluded that stimulation of sensoTy nerves (central end of the 

 sciatic) increased the output of epinephrin. Anrep(&, ~b) stated that if the 

 nerves of a hind limb or a kidney (in the dog) be cut, these denervated 

 parts respond to stimulation of afferent nerves (central end of sciatic) 



