SIGNIFICANCE OF THE SUPRARENAL GLANDS 147 



accumulation of epinephrin in the glands is, therefore, accelerated as 

 well as its liberation. As already mentioned, the action is well obtained 

 after section of the cord anywhere in the cervical region, but not after 

 division of the efferent secretory path (splanchnics, etc.). It is, there- 

 fore, a central action (on the thoracic cord). Indications were found in 

 some experiments that the state of prolonged augmentation of the rate 

 of output, which constitutes the principal action of the drug, may be pre- 

 ceded by a transient diminution, best seen with the smaller doses and 

 with subcutaneous administration, presumably because with the larger 

 doses and with intravenous injection the augmentation of the output 

 comes on so rapidly as to mask any preliminary decrease (Stewart and 

 Rogoff, 1919('in). The increase in epinephrin output produced by the 

 intravascular injection of small volumes of concentrated salt solutions 

 (sodium carbonate), accompanied by symptoms of a general excitation of 

 the bulbospinal centers, is probably due, like the strychnin increase, to 

 excitation of the central epinephrin secretory mechanism. 



The action of nicotin is, speaking generally, the converse of the 

 strychnin effect. Dale and Laidlaw observed that certain reactions, which 

 are elicited by this drug on the non-pregnant uterus of the cat and in the 

 eye after removal of the superior cervical ganglion, are modified when the 

 experiment is made under such conditions that epinephrin can no longer 

 reach these structures from the suprarenals. They explained the difference 

 by the hypothesis that the nicotin action is in part due to a stimulation of 

 the suprarenals to increased liberation of epinephrin. Gley(fr) (1914) con- 

 cluded that the rise of blood-pressure caused by nicotin in dogs with the 

 spinal cord and bulb destroyed is practically due entirely to the increased 

 outpouring of epinephrin. But such a rise of pressure as he saw (e.g., 

 from less than 30 mm. to 140 mm. of mercury in a dog) is far too great 

 to have been caused by any increased output of epinephrin due to nicotin, 

 and was undoubtedly largely due to excitation of the sympathetic ganglion 

 cells on the vasomotor path (see Laiigley, 1918(&)). 



Cannon, Aub and Binger, stated that "injection of nicotin in small 

 amounts (3.5 to 7.5 mgm. in cats) results in augmented suprarenal secre- 

 tion/ 7 which is evident in samples of blood obtained 3 or 4 to 10 or 12 

 minutes after administration of the drug. It is impossible, however, by 

 the method used (collection of blood by a catheter from the inferior vena 

 cava above the level of the suprarenal veins) to arrive at any conclusion as 

 to the effect of the drug upon the rate of output of epinephrin. For 

 changes in the rate of the blood flow were not taken account of, and it is 

 TO be expected that the concentration of epinephrin in the suprarenal blood 

 and, therefore, in the caval blood above the suprarenal veins, may be inr 

 creased at some stage after the injection of such doses of nicotin, owing 

 to the diminution of the rate of blood flow associated with a marked and 

 prolonged fall of blood-pressure succeeding the brief rise. But such an 



