RELATION SUPRARENAL GLANDS TO CIRCULATION 223 



having a 2:1 rhythm they administered small doses of the drug and re- 

 ported that the dissociation almost entirely disappeared in four minutes. 

 Other observers, however, have not been able to substantiate this claim. 

 Hardoy and Houssay (1917) administered epinephrin to a dog with experi- 

 mental heart block and to two patients. They found that both the auricles 

 and the ventricles were stimulated but in different degrees. It so hap- 

 pened that the changed rhythms caused the auricular and ventricular beats 

 occasionally to assume a normal temporal relationship to each other and 

 thus brought about the appearance of brief reconstitution of the normal 

 rhythm. Arrillaga (1919) studied six cases of clinical auriculo-ven- 

 tricular dissociation by means of the electrocardiograph. Reconstitution 

 of the normal rhythm was not observed in any case. Ordinarily the reac- 

 tion of the auricles and ventricles occurred simultaneously, but occasion- 

 ally the ventricles reacted first. This observation is of interest in that it 

 confirms in man the fact noted in the various experimental animals that 

 epinephrin acts not merely upon the "pace-maker" but upon the auricles 

 and ventricles more or less independently. 



In man, as will be discussed in subsequent paragraphs, epineph- 

 rin ordinarily produces acceleration of the pulse. In dogs deeply 

 anesthetized, especially if morphia is used, a similar acceleration is 

 sometimes noted. In the laboratory animals generally, however, under 

 conditions of ordinary anesthesia, the usual effect is depression of the 

 pulse rate. This probably results to a considerable extent from reflexes 

 set up by the high blood-pressure, particularly in the proximal aorta, which 

 are mediated through the vagus nerve. That the high blood-pressure is 

 not the only cause of the slowing, however, has been shown in different 

 ways. Brooks, McPeek, and Seymour (1918) interposed in the blood- 

 stream a reservoir bottle connected with the aorta. Under conditions 

 which ordinarily would produce a rise in arterial pressure, blood flowed 

 into the reservoir and the pressure was thus kept at approximately a con- 

 stant level. It was shown that epinephrin injected under such conditions 

 caused both slowing of the heart and increased amplitude of the beat. 

 Brown (1916) studied the effect of epinephrin applied to the vagus center 

 directly. He perfused the medulla of dogs with a mixture of defibrinated 

 blood and saline solution through the carotid and vertebral arteries. When 

 epinephrin was introduced into the perfusion mixture, slowing of the 

 heart occurred immediately, before any reflex mechanisms resulting from 

 changes of blood-pressure could come into play. Heinekamp (1919) car- 

 ried out somewhat similar experiments with turtles. He perfused the head 

 independently, leaving it connected with the body only through the vagus 

 nerves. The introduction of epinephrin under these conditions also caused 

 slowing of the heart. 



Reaction of human subjects to epinephrin has been studied extensively 

 by clinicians in recent years, Clough (1920) has summarized the Htera- 



