356 Dr. W. M. Bayliss. On Recoprocal [Jan. 20, 
arterial pressure being due to those in the majority. The reason why the 
effect, in the complete animal, of the first and second doses is opposite is, in 
all probability, that the alkaloid, after strongly exciting the constrictor 
mechanism, paralyses this earlier than it does the dilator. It will be shown 
later that the toxic action is not on the efferent vaso-constrictor neurone; it 
may be on the synapse of the pressor fibre or of an intermediate neurone 
with the cell-body of the former, or even earlier on the afferent side. 
In this connection the fact is of interest that, after strychnine, there is no 
rise of blood-pressure in asphyxia; there is, on the contrary, an excitation of 
dilators, as shown by fig. 13. The dilatation seen comes on too early to be an 
effect of raised venous pressure. Since the constrictor neurone itself is not 
Fic. 13.—Asphyxia after strychnine. Upper curve, volume of penis. Lower curve, 
arterial pressure. At the time when the tracing begins the artificial respiration 
was stopped. 
attacked, a fact shown by the persistence of vaso-constrictor effects from the 
depressor, it follows that the action of asphyxial blood in exciting con- 
strictors is not exerted directly on the efferent neurone itself. In normal 
animals, I at times observed dilator effects in asphyxia. These do not appear 
to be due to the direct action of carbon dioxide on the blood-vessels,* since 
they were not to be seen in organs deprived of their dilator supply. 
That the constrictor mechanism, or rather the afferent excitor part, is 
paralysed by strychnine in smaller dose than is required by the dilator 
mechanism, is also confirmed by the fact that the first dose of the drug is 
usually sufficient to abolish all pressor effects from the central end of an 
ordinary sensory nerve. 
Cocaine produces a rise of arterial pressure by central excitation of con- 
* Bayliss, ‘Physiol. Soc. Proc.,’ 1901, p. xxxii. In ‘Journ. of Physiol.,’ vol. 26, 1901. 
