PHARMACOLOGY OF EPINEPHRINE 133 



tion of the liver directly. Epinephrine can thus not be held 

 responsible for the hyperglycemia following decerebration, al- 

 though it may play some part in bringing it about. 



OTHER PHARMACOLOGICAL EFFECTS OF EPINEPHRINE 



Epinephrine also causes other detectable changes in the 

 animal economy but these are inconsiderable in their effects 

 and for the most part are probably secondary to the influences 

 described in preceding sections. Changes in acid-base balance, 

 in salt metabolism, in blood concentration, et cetera have been 

 described. 639 



As first noted by Vosburgh and Richards, 651 the injection of 

 epinephrine shortens the coagulation time of the blood. Can- 

 non and Gray 104 found the intravenous injection of 0.001 

 mgm. per kilo to shorten the time to one-half to one-third of 

 the normal. This action is due to the liberation from the liver 

 of substances concerned in the process of coagulation. Large 

 doses inhibit coagulability. These effects presumably result 

 from the action of epinephrine on the liver for epinephrine 

 when added to shed blood does not affect coagulation. 



The possible influence of epinephrine on protein metabolism 

 is still debatable despite a number of investigations designed 

 to determine this relationship. 



TOXICOLOGY OF EPINEPHRINE 



Large doses of epinephrine produce violent symptoms which 

 may end in death. At first there is a period of excitement with 

 rapid pulse and respiration. This reaction has occasionally 

 been obtained in man where an intended subcutaneous injec- 

 tion has been accidentally introduced intravenously. Follow- 

 ing the period of excitement, depression supervenes. The ani- 

 mal lies on its side, muscular movements are slowed, and 

 paralysis of the limbs follows. The animal becomes dyspnoeic 

 and finally dies in asphyxial convulsions. The paralysis is 

 central, death being due to pulmonary edema. 



