400 
stimulation of the vagus any relawation of the contracted 
ventricle took place, but on this point he is not sure. 
These results at first sight seem identical with the phe- 
nomena observed by Schmiedeberg' in nicotin poisoning (Lud- 
wig’s Arbeiten, 1870, p. 41), and explained by him as due to 
accelerator fibres in the vagus of the frog. 
The author is unable to accept this explanation: 
1. Because both inhibition and secondary action fail 
when atropin is given with the antiar (the antiar otherwise 
acting as usual). 
2. Because a similar secondary action may be seen in all 
cases of inhibition not only of the frog’s heart but also of the 
mammalian heart in which the accelerator fibres are supposed 
to run not in the vagus. 
3. Because a similar secondary action may be seen in 
the snail’s heart after inhibition by direct application of the 
interrupted current, and in certain conditions of the snail’s 
heart may be witnessed when the inhibition cannot be de- 
tected. 
The author regards the secondary action as being what for 
want of more precise knowledge he would call “a reaction” 
following the direct action of the vagus. And considering that 
antiar acts essentially, or at least primarily, on the muscular 
tissue of the heart, the peculiar prominence of this reaction in 
antiar poisoning may be taken as indicating on the one hand 
that the effects of antiar are especially favourable to this reac- 
tion, and on the other that the vagus nerve brings about 
inhibition by acting directly on the muscular tissue itself—a 
view which is supported by other facts. 
