2OO INTERNAL SECRETION 



that the effect of adrenalin upon the vascular muscles depends 

 upon their vaso-motor innervation. The treatment, with adrenalin, 

 of portions taken from the coronary vessels of the ox is followed, 

 not by shrinking, but by a distinct lengthening of the specimens. 

 In this instance, therefore, adrenalin does not provoke contraction 

 but dilation. This result is explicable if we take into consideration 

 the fact that the sympathetic innervation of all peripheral vessels 

 is constrictor, while, according to P. Maass, the sympathetic 

 nerves supplying the coronary vessels of the heart (which include 

 the first thoracic ganglion and the ansa Vieussenii) contain only 

 dilator fibres, the contractors being conveyed by the pneumo- 

 gastric nerve. 



It may be noted in passing that the antagonism, which 

 Langendorff discovered between the cardiac vessels and the other 

 peripheral vessels, is demonstrable by means of substances other 

 than adrenalin. Eppinger and Hess found that, unlike adren- 

 alin, pilocarpin, physostigmin and cholin hydrochlorate (Merck) 

 produce a shrinking that is to say, a contraction of portions 

 taken from the coronary vessels, while in the case of the peri- 

 pheral vessels, they induce dilation as shown by the increase in 

 length. Certain substances influence both sets of vessels in the 

 same manner, barium chloride, calcium salts and the digitalis 

 bodies producing contraction, while atropine, ergotin and the 

 nitrites produce dilation. According to Pal, pilocarpin contracts 

 the coronary, mesenteric and femoral arteries and dilates the renal 

 artery. 



The observations described above justify the conclusion that 

 the site of the influence of adrenalin is to be sought, not in the 

 muscular structure of the vessels, but in those apparatuses which 

 are in communication with the sympathetic nerve endings. 



The Heart. As we now know, the full effects of adrenalin 

 upon the heart are to be seen only after the inhibitory vagal 

 nerve endings have been paralysed by means of atropine. If the 

 vagi are allowed to remain intact, the predominant effect will be 

 the slowing of the rhythm, due to the increased arterial tension. 

 Even the resection of the vagi at the neck does not entirely over- 

 come the tendency to a retarded rhythm, interrupted by single 

 arhythmic beats. The slowing of the pulse and the extra-systolic 

 arhythmia are sufficiently explained by the increased venous ten- 

 sion and consequent impossibility of completely emptying the left 

 ventricle. 



The full action of adrenalin may, however, be observed in 

 the mammalian heart in situ after the vagal terminals have been 

 paralysed with atropine. There is, as a rule, a further accelera- 

 tion of the contractions and there is, especially, a stronger ventri- 

 cular systole which is well seen by registering the contractions 

 or by means of a plethysmograph. This increased cardiac activity 

 is the result, not of improved circulatory conditions arising out 





