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therefore, a priori, to be expected that the phenomena of mechanical and of nitrous oxide
asphyxia should differ to a certain extent. To determine the way in which nitrous oxide
inhalation affects the circulation, I have, during the past winter, in connection with my assist
-ant and friend, Dr. David Gerna, made a long series of experiments. The result has been to
show that usually the inhalation is followed by a rise of the arterial pressure, accompanied by
a great disturbance of the pulse; the pulse at first becoming irregular and tumultuous, but
by-and-by settling, so that when anæsthesia is complete the pulse wave is remarkably large
and full, and the rate very slow. The rise and fall of the arterial pressure in nitrous oxide
anæsthesia was found to vary remarkably, not only in different inhalations, but in different
periods of the same inhalation. Sometime the rise was sudden, sometimes it was slow and
gradual; sometimes it was maintained until near death, sometimes it was interrupted very
early; sometimes it was not very well marked, sometimes it was enormous.
In all our experiments respiration ceased while the heart was still in full activity.
Indeed, instead of the gas acting as a cardiac depressant, it appeared to act as a cardiac stim
u-lant, although it paralysed the vaso-motor apparatus. Thus, during complete anæsthesia, fara
-disation of the sciatic nerve always failed to register in an increase of the blood-pressure,
although the heart was beating very powerfully, and although the pneumogastrics had been
previously severed: whilst late in the poisoning—at a time when the respiration had abso
-lutely ceased, and the animal was in this respect dead, and without the power of self-recovery,
and when the arterial pressure also had fallen almost to zero—the pulse waves were frequently
still nearly three times the normal.
We made but few experiments as to the action of artificial respiration upon the animal
dyi ng f r om ni t r ous oxi de, but t hese exper i ment s pr oved t hat even af t er compl et e par al ysi s of
the respiratory function, artificial respiration is capable of rapidly bringing the animal back
to life. The heart lives on through nitrous oxide anæsthesia long after the respiratory function
has been abolished, and even when the strong, full pulse fails, and the heart has almost ceased
to quiver, recovery is still hopeful, because the loss of function has been caused, not by the
presence of a poison, but by the absence of oxygen; and although the paralysis may be com
-plete, the life power sleeps before it dies, and is ready to awake at the touch of fresh oxygen.
These experimental results are in strict accord with clinical observations. The S. S.
White Dental Manufacturing Company supply a very large, if not the largest portion of the
apparatus and material used for the administration of nitrous oxide in the United States; and,
in answer to my inquiry, Dr. J.W. White, their President, writes me that a computation
based upon their own sales, and a knowledge of those of their rivals, has reached "the some
- what appal l i ng r es ul t , t hat anæs t hes i a by ni t r ous oxi de gas i s pr obabl y ef f ect ed i n t hr ee- quar t er s
of a million of cases annually in the United States". Most of these inhalations have been
given, not by trained physicians, but by comparatively untrained and often very ignorant
dentists; have been given to patients in a sitting or semi-sitting posture; have been given
apparently without thought or care to the general community, as the units presented themselves
to the healthy and to the diseased alike; and the result is, out of many millions of inhalations,
only three deaths recorded as directly due to nitrous oxide. Could anything be safer?