1908. | Innervation in Vaso-motor Reflexes, ete. 375 
alkaloid, the synapse of the press or fibres with the constrictor centre being 
the first to show paralysis as the dose is increased. 
8. In the “dilator” animal strychnine causes a fall of hibed> -pressure on 
injection by exciting dilator centres. In the normal animal the first dose 
causes a rise and subsequent ones a fall of pressure, since the first dose, if 
not too small, after exciting the vaso-constrictor centre, paralyses the synapses 
concerned, so that the simultaneous excitation of the dilator centres can now 
make itself felt. 
9. The excitation of constrictors produced by reversal of inhibition is more 
resistant to the alkaloid than that produced in the normal way. 
10. Asphyxial blood does not act directly on the efferent constrictor 
neurones, since it has no action at a stage of strychnine poisoning at which 
the depressor still excites constriction, by reversal of inhibition. 
11. Chloroform converts pressor into depressor reflexes (in the rabbit), by 
reversal of excitation of constrictors into inhibition. 
12. This effect of chloroform is not exerted on the efferent neurones 
directly, but at some point considerably earlier in the reflex arc. This is 
shown by the fact that asphyxial blood causes rise of pressure when excitation 
of sensory nerves causes fall. 
The expenses of this research were partially defrayed from the Government 
Grant administered by the Royal Society. 
[Note added March 23, 1908.—Since the preceding paper was written, I 
have received from Professor Mislavsky, of Kasan, a number of tracings 
showing a dilatation of the tongue of the dog and cat on excitation of the 
central end of the vagus, after section of the cervical sympathetics above the 
superior cervical ganglia. In one case there was no obvious change in the 
blood-pressure, a fact which perhaps makes the reflex origin of the dilatation 
somewhat doubtful; in the other cases there was the usual fall. In all cases, 
as Professor Mislavsky informs me, the effect was abolished by section of the 
lingual nerves, so that there seems no doubt that it was due to excitation of 
vaso-dilator fibres. These experiments were performed by Professor 
Mislavsky in conjunction with his pupil, Mr. Fofanoff. 
The results are of interest, in that they bring evidence of dilator-excitation 
in an organ on which my own experiments had been only partly successful. ] 
