224 E. G. HOSKINS 



ture and added numerous observations of his own. It is found that there 

 is a marked difference in the cardiovascular reaction of different subjects 

 to epinephrin when injected either subcutaneously or intramuscularly. 

 The dosage has usually been 0.5 or 1.0 mg. Clough has classified the 

 reactions arbitrarily, according to their intensity, as negative, moderate, 

 marked, and very marked. In the moderate reaction there was a rise of 

 systolic blood pressure of from 15 to 30 mm. of Hg associated usually 

 with a fall of from 10 to 20 mm. in diastolic pressure. The striking 

 feature of the reaction was the increase in pulse pressure which was 

 often doubled. Despite the increased blood pressure, the pulse was usually 

 quickened. In marked reactions the systolic pressure rose from 30 to 100 

 mm. There was usually a slight rise in diastolic pressure also and a 

 marked rise in pulse pressure. When atropin was administered to block 

 the vagus impulses, the reaction was often augmented. Further details 

 regarding the effect of epinephrin on the pulse rate will be found in the 

 chapter, "Clinical Tests for Thyroid Disorders." 



In view of the stimulating effect of epinephrin upon the heart as a 

 whole, its effect on the coronary circulation is of particular interest. A 

 priori, dilatation would b expected in order to afford a greater blood 

 supply to the cardiac muscle during the period of increased activity. Per- 

 fusion experiments by the earlier investigators showed that dilatation 

 results in most experimental animals from the application of epinephrin. 



Simple perfusion experiments in themselves are not, however, entirely 

 conclusive, since the coronary flow may be influenced more or less by the 

 reaction in other parts of the cardiovascular system. Morawitz and 

 Zahn(a) (b) restiulied the problem in the intact animal, using hirudinized 

 cats and clogs as subjects. A catheter was inserted through the right 

 auricle into the coronary sinus. The blood thus collected, after being 

 measured with a recording device, was returned to the jugular vein. Epi- 

 nephrin was found to cause augmented flow quit out of proportion to the 

 increase in general arterial pressure. 



Barbour (1912) obtained evidence, however, that in man epinephrin 

 exerts a different effect upon the coronary arteries from what it does in the 

 laboratory animals. It was demonstrated that isolated rings of the coro- 

 nary arteries, obtained from subjects shortly after death, responded to 

 epinephrin by contraction only. The experiments were controlled by the 

 use of similar rings from calves, sheep, and pigs. These all responded by 

 relaxation. 



In view of the somewhat anomalous reaction observed in man, Barbour 

 and Prince (1915) reinvestigated the problem in another primate, the 

 Macacus rhesus, the experiments being controlled with rabbits. Isolated 

 hearts were employed, these being perfused with diluted blood to which 

 hirudin was added. The heart was excised immediately after death and 

 connected with the aortic cannula of the perfusion system. Injections of 



