SIGNIFICANCE OF THE SUPRARENAL GLANDS 145 



in animals dying in asphyxial convulsions the spinal epinephrin secretory 

 mechanism, like the spinal motor mechanisms, would he excited so much 

 as to cause a marked increase in epinephrin output is unknown, as it is 

 difficult to collect blood for a satisfactory assay when the flow is greatly 

 slowed. 



vAA^ 



y v / 



F/ 



A'.ltf. 



2SS 



151 



Fig. 17. Blood pressure tracings from cat after section of vagi and excision of 

 stellate ganglia. A, before asphyxia; B, a portion just before the end, and C, a portion 

 commencing 18 seconds after the end of a 45 second period of asphyxia, before tying 

 off all the blood vessels of the suprarenals. The preliminary dissection had already 

 been made and ligatures placed in position. D, before asphyxia; E, a portion just 

 before the end of asphyxia, and F, a portion commencing 27 seconds after the end of a 

 45 second period of asphyxia, after the suprarenal vessels had been tied off. The num- 

 bers give the pulse rates and show that the acceleration of the denervated heart asso- 

 ciated with asphyxia was quite as great after elimination of the suprarenals as while 

 they were discharging epinephrin. Accordingly the acceleration caused by asphyxia is 

 not due to increased output of epinephrin from the suprarenals. Time trace, seconds. 

 (After Stewart and Kogoff, Am. J. Phijsiol) 



Cannon's(e)(1919) experiments on the heart, assumed to he isolated 

 from the central nervous system by section of the vagi and excision of the 

 stellate ganglia (in cats), do not throw any light upon the question 

 whether it is possible to demonstrate an augmented epinephrin output due 

 to sensory stimulation, asphyxia, or emotion. For it has been shown by 

 Stewart and Rogoff(^) (1920) that, the reaction upon which he relies, ac- 

 celeration of the heart, does not depend upon increased epinephrin output 



