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The mouth and nose were not closed till 12h. 17m. 35s.—just five seconds before the end
of, and therefore too late to produce any marked effect in, the Fick reading. But the
effect is well shown in the continuation of the observation on the Ludwig manometer. The
Glasgow Committee have had every possible opportunity of examining the original tracings,
and an inaccurate quotation such as that which I have called attention to is no less misleading
than it is, from a scientific point of view, indefensible.
I make no comment on the comparison of the Commission's Experiment 148 with
the Glasgow trace. All the tracings of Experiment 148 are published above, and anybody
can form his own opinion about them, and about the Committee's observations on them.
The Committee next confuse the fall of pressure due to ordinary chloroform inhalation
with the fall due to interference with the respiration. The Hyderabad Commission have
stated that the fall of pressure and slowing of the pulse, from either involuntary holding of the
breath or from asphyxia in chloroform inhalation, are due to vagus stimulation, reflex or
direct. The Commission has given no opinion as to the cause of the fall produced by diluted
chloroform alone. It is obvious, from all their experiments, that the effects of chloroform
are first exerted upon the nervous tissues, the vaso-motor centre is very soon involved, the
respiratory centre becomes paralysed, then the muscular tissues become affected, and last of
all the heart. The fall of blood-pressure becomes dangerous if pushed to the point of paralysis
of the respiratory centre. After this point is passed, if the poisoning with chloroform still
continues, the fall becomes much more rapidly dangerous; the nutrition of the heart is
profoundly interfered with, and the deprivation of oxygen produced by the paralysis of the
respiratory centre causes it to gradually cease to act. The Glasgow Committee contend that
"when chloroform is pushed, whether the mouth and nose be held or not, the blood-pressure falls,
and there is the additional fact that this seems to depend very little on the action of the vagi".
In support of this contention—which the Hyderabad Commission do not altogether dispute—the
Committee quote from Fick readings 3 and 6 of Experiment 151. But Fick 3 of No. 151 is
a reading during simple smothering, the vagi being intact. The effect of the smothering is to
almost immediately lower the pressure about 25 millimêters, and to slow the pulse from 72 to
31 per minute at the same time. After the vagi are cut, when asphyxia is again produced by
smothering (vide Fick 6), the effect is to accelerate the pulse to 105 per minute, while the
pressure only falls about 5 millimêtres. This difference is most assuredly due to the division
of the vagi, and yet the Committee assert that the slight fall with rapid pulse in Fick 6 is
" the true asphyxia curve", and depends "very little on the action of the vagi". In this con-
nection, it may be well to notice what the Galasgow Committee have to say with regard to
atropine. The Committee refer to the Hyderabad Commission's discovery of the safeguard
action of the vagus, in chloroform poisoning, and remark that when the inhibitory action of
the vagus is brought into play less chloroform is conveyed to the nerve centres; and, further,
if vagus irritation ceases, or the nerve becomes exhausted, the heart "bounds on again, and
the blood then becomes very quickly saturated with chloroform, and an overdose is at once
conveyed to the nerve centres". The Committee continue: "This ingenious view has much
to support it", and "it undoubtedly explains the beneficial action of atropine as an adjunct to