SIGNIFICANCE OF THE SUPRARENAL GLANDS 149 



output are roughly parallel to the changes in the blood-pressure caused by 

 nicotin, indicating that when the sympathetic ganglion cells on the efferent 

 vasomotor path are being stimulated or depressed, a corresponding stimu- 

 lation or depression is being exerted on the efferent suprarenal secretory 

 path. The transient augmentation of the epinephrin output may be as- 

 sociated with an increase in the concentration of epinephrin in the supra- 

 renal vein blood much beyond the maximum seen with the slowest 

 blood flow in animals simply anesthetized with ether, morphin, or 

 urethane (Fig. 19) so that epinephrin may even be detected in the serum 

 by the colorimetric test of 

 Folin, Cannon and Denis. 

 The strychnin augmenta- 

 tion of the output has not 

 been observed to be associ- 

 ated with any distinct in- 

 crease in the normal maxi- 

 mum concentration (some- 

 thing like 1 :500,000 in the 

 serum of suprarenal vein 

 blood, assayed with rabbit 

 segments) so long as the 

 connection of the thoracic 

 cord with the upper parts of 

 the central nervous system 

 remains unbroken. But 

 when strychnin is adminis- 

 tered after section of the 

 cervical cord the increased 

 epinephrin output may be 



Fig. 20. Blood pressure tracing from a cat. At 

 5, a two minute cava pocket (before injecting nico- 

 tin) was released; at 9, a two minute pocket, dur- 

 ing the period of closure of which was injected 1 

 mgm. nicotin, was released; at 11, a two minute 

 pocket (seven minutes after the nicotin injection) 

 was released. The output of epinephrin was ob- 

 viously increased at 9 and depressed at 11. Zero 

 line corresponds with time trace and is moved up 

 30 mm., and the figure then reduced to two-thirds. 

 Time trace shows 10 second intervals. (After Stew- 

 art and Rogoff, /. Pharm. d Eocper. Therap.) 



associated with extremely 



high concentrations of epinephrin (as much as 1 : 100,000 or even more in 

 the suprarenal blood). A hypothesis which would explain this is that a 

 center exists in some part of the central nervous system above the level of 

 the thoracic cord which exerts an inhibito-regulatory influence upon the 

 output. The transient preliminary diminution in the output caused by 

 strychnin may be due to excitation of this mechanism, the subsequent 

 increase being brought about by stimulation of the thoracic spinal 

 mechanism. 



Curare in doses sufficient to paralyze the skeletal muscles of the cat 

 markedly depresses the output of epinephrin from the suprarenals. 



It was stated by Ehrmann (b) (1906) that atropin and pilocarpin cause 

 no alteration in the quantity of epinephrin in the blood of the suprarenal 

 veins. He refers only to the concentration of the epinephrin. He did 

 not take account of possible changes in the blood flow, and his method 



