98 THE SIMPLER NATURAL BASES 



of a large number of related amines) resembles that of the sympathetic 

 nervous system and has accordingly been termed by Dale [Barger and 

 Dale, 1910, i] " sympathomimetic ". Adrenaline does not, however, 

 affect the sympathetic nerves themselves, for, as has been shown by Lew- 

 andowsky [1899, 1900], Langley[ 1901] and Elliott [1905], the reactivity 

 of plain muscle to adrenaline is not diminished (but rather increased) 

 by cutting the sympathetic nerve supply and allowing the nerves to de- 

 generate. Moreover apocodeine, as Dixon has shown, abolishes the 

 excitability of muscle by sympathetic nervous impulses, and by 

 adrenaline, but leaves all other irritability unaffected. The blood 

 vessels of the lungs, which have no sympathetic innervation, are on 

 the other hand not affected by adrenaline, according to Brodie and 

 Dixon [I9O4]. 1 In order to account for the persistence of the 

 adrenaline action after degeneration of the sympathetic nerve supply, 

 Elliott [1905] has invoked a hypothetical structure, the " myo- 

 neural junction," which does not degenerate with the nerve and is the 

 seat of the action of adrenaline. Langley's conception of a " receptive 

 substance " for adrenaline is in most essential respects identical with 

 Elliott's. The nature of the myo-neural junctions determines the re- 

 sponse to adrenaline, i.e. whether inhibition or augmentation takes 

 place. Thus these structures would differ in different animals ; in some 

 species the augmentor elements would predominate, so that adrenaline 

 causes contraction, in others the reverse condition would prevail. Simi- 

 larly, during pregnancy, in the cat, the augmentor elements of the 

 uterine myo-neural junctions would achieve preponderance over the 

 inhibitor elements, which predominate in the non-pregnant animal. 



The existence, side by side, of two kinds of elements, augmentor 

 and inhibitor, receives considerable support from the discovery by 

 Dale [1906], that the alkaloid ergotoxine paralyses one set of 

 elements without greatly affecting the other. Thus the large rise of 

 blood pressure which adrenaline causes in the normal animal is replaced 

 by a (smaller) depressor effect, if ergotoxine has been previously ad- 

 ministered. The ergotoxine paralyses the augmentor elements only 

 (which normally overcome the inhibitor effect) so that, after ergotoxine, 

 the inhibition becomes evident and a " vaso-motor reversal " occurs. 



1 A different conclusion was reached by Wiggers [1909] who attributes Brodie and 

 Dixon 's results to their use of a perfusion fluid of smaller viscosity than that of the blood. 

 Older experiments of Plumier and of Langendorff also indicate that adrenaline causes 

 the pulmonary vessels to contract, but Cow [1911] using O. B. Meyer's method (p. 103) 

 finds that the intravisceral portion of the pulmonary, the cerebral and the coronary arteries 

 are not constricted. The action of adrenaline on the pulmonary vessels has also been 

 studied by Baehr and Pick [1913, 2, Ch. I]. 



