RELATION SUPRARENAL GLANDS TO CIRCULATION 201 



level to 65 mm., the reaction was converted to the pressor type. Defibrin- 

 ated blood was then injected and, as the pressure gradually rose, the de- 

 pressor epinephrin reaction reappeared. 



Hartman and his collaborators have more recently published extensive 

 observations upon the epinephrin vasodilator mechanisms. They noted 

 that if the splanchnic nerves were cut epinephrin, which had previously 

 caused vasoconstriction, now caused only dilatation. This observation led 

 to a study of the part played by the central nervous system. Their experi- 

 ments were made upon dogs and cats, the volume changes in the intestine 

 and in normal or denervated limbs being recorded along with systemic 

 blood-pressure. Simultaneous records were made of the volume changes 

 in the two hind-limbs after one had been denervated. Gruber's observa- 

 tion to the effect that small doses of epinephrin usually gave dilatation 

 in the normal limb and constriction of the denervated structure was con- 

 firmed. Large doses, however, such as those which usually produce a rise 

 in blood-pressure, caused constriction in both limbs. This was true in 

 ten of fifteen cats. The dilatation in the denervated limb appeared to be 

 passive since it occurred at the same time blood-pressure began to rise and 

 persisted an equal length of time. Such dilatation was cut short or ob- 

 viated with large doses of epinephrin. Dilatation in the normal limb came 

 later than in the denervated and lasted as long as the blood-pressure was 

 below normal. 



It might be assumed that the failure to evoke dilatation in the dener- 

 vated limb was due to extreme relaxation of the blood-vessels incident to 

 loss of tonic impulses. By the use of a substance obtained from ox 

 pituitaries, however, it was shown that such was not the case, marked 

 dilatation occurring in both normal and denervated limbs. 



The foregoing observations indicated that the central nervous sys- 

 tem plays a considerable part in the vasodilator reaction to epinephrin. 

 This was further shown in another way. A segment of intestine or a limb 

 was cut off from the body circulation and independently perfused with 

 warm oxygenated Ringer's solution. The part was left in connection with 

 the central nervous system through its normal nerve paths. The organ 

 was then placed in a plethysmograph and volume changes noted, or the 

 outflow was measured directly. Injections of epinephrin were then made 

 into the body circulation, proper, and the effects upon the organ in ques- 

 tion noted. It was found that clean-cut vasodilator effects could readily 

 be elicited. Since the only connection between the perfused organ and 

 the remainder of the body was by way of the nerve paths, the vasodilatation 

 must have been mediated by the central nervous system or the sympathetic 

 ganglia (Fig. 3). 



That the nervous mechanism involved in this reaction was below the 

 cerebrum was proved by the fact that the destruction of this organ failed 

 to abolish the reaction; likewise it failed to prevent the fall in blood- 



