1908. | Innervation in Vaso-motor Reflexes, etc. 369 
chloroform, on the constrictor centre, the normal excitation becoming 
inhibition. In curve D a second similar dose was given: the first effect was 
again a fall, the chloral was not yet fully antagonised, but, after a short time, 
this was effected and the alkaloid now produced its usual excitatory effect. 
Moreover, excitation of the anterior crural also had its ordinary result, a rise 
of pressure (curve E). 
Asphyxial blood is capable of causing rise of pressure and peripheral vaso- 
constriction under a dose of chloroform which reverses the effect of exciting 
a sensory nerve. This fact proves that the action of chloroform is not 
exerted on the efferent neurone itself, at least not as regards its effect in 
converting excitation into inhibition. 
When electrodes are placed on the floor of the fourth ventricle, over the 
situation of the so-called vaso-motor centre, it is found that, in the rabbit, 
chloroform converts the usual pressor effect into a depressor one. It might be 
thought that this result is at variance with the view here taken as to the action 
of this drug. It seems unlikely that direct electrical excitation of the efferent 
neurone should cause inhibition of it. On the other hand, it is much more 
probable that, by this means, afferent tracts to the centre are excited, rather 
than the centre itself. So that the experiment is merely a variant of excita- 
tion of ordinary sensory nerves. 
It is remarkable that the chloroform reversal cannot be obtained in the cat. 
I have seen a slight rise followed by a fall of pressure, but this latter proved, 
on examination, to be due to slowing of the heart, although the vagi were cut. 
It was, presumably, due to the enfeebled heart not being able to work under 
the raised pressure. In fact, the heart seems to fail before a dose of the drug 
has been given sufficient to effect change of excitation into inhibition. 
As is well known, administration of chloroform is followed by fall of 
arterial pressure; this 1s usually attributed to failure of the heart’s action, 
and, no doubt, this is the main factor, but I have several times observed, 
in plethysmographic tracings of both intestine and limb in the initial stage 
before the pressure has fallen to any great extent, an unmistakable dilatation 
of the peripheral vessels. This comes on too early in the fall of pressure to 
be due to rise of venous pressure and it gives place to a passive diminution of 
volume as the blood-pressure continues its downward course. It is possible 
that this dilatation may be produced by direct action of the drug on the 
arterioles; it is more probable, I think, that it is of central origin and 
brought about in this way: afferent pressor stimuli are continually being 
received by the constrictor centre, and are, to some degree at all events, the cause 
of its normal state of tonic excitation. Under chloroform these stimuli cause 
inhibition of constrictor tone, and, therefore, dilatation of peripheral vessels. 
