The discovery of the anesthetic properties of ether and
its practical application to surgery must always stand as
one of the great achievements of medicine. It is eminently
fitting that the anniversary of that notable day, when the
possibilities of ether were first made known to the world,
should be celebrated within these walls, and whatever the
topic of your Ether Day orator, he must fittingly pause first
to pay tribute to that great event and to the master surgeons
of the Massachusetts General Hospital. On this occasion,
on behalf of the dumb animals as well as on behalf of suffering
humanity, I express a deep sense of gratitude for the
blessings of anesthesia.
Two years ago, an historic appreciation of the discovery
of ether was presented here by Professor Welch, and last
year an address on medical research was given by President
Eliot. I, therefore, will not attempt a general address, but
will invite your attention to an experimental and clinical
study. In presenting the summaries of the large amount of
data in these researches, I acknowledge with gratitude the
great assistance rendered by my associates, Dr. D. H.
Dolley, Dr. H. G. Sloan, Dr. J. B. Austin, and Dr. M. L.
Menten.
[2]
The scope of this paper may be explained by a concrete
example. When a barefoot boy steps on a sharp stone there
is an immediate discharge of nervous energy in his effort
to escape from the wounding stone. This is not a voluntary
act. It is not due to his own personal experience—his
ontogeny—but is due to the experience of his progenitors
during the vast periods of time required for the evolution of
the species to which he belongs, i. e., his phylogeny. The
wounding stone made an impression upon the nerve receptors
in the foot similar to the innumerable injuries which gave
origin to this nerve mechanism itself during the boy's vast
phylogenetic or ancestral experience. The stone supplied
the phylogenetic association, and the appropriate discharge
of nervous energy automatically followed. If the sole of the
foot be repeatedly bruised or crushed by a stone, shock may
be produced; if the stone be only lightly applied, then the
consequent sensation of tickling causes a discharge of nervous
energy. In like manner there have been implanted in
the body other mechanisms of ancestral or phylogenetic
origin whose purpose is the discharge of nervous energy for
the good of the individual. In this paper I shall discuss the
origin and mode of action of some of these mechanisms and
their relation to certain phases of anesthesia.
The word anesthesia—meaning without
feeling—describes
accurately the effect of ether in anesthetic dosage. Although
no pain is felt in operations under inhalation anesthesia, the
nerve impulses excited by a surgical operation still reach the
brain. We know that not every portion of the brain is fully
anesthetized, since surgical anesthesia does not kill. The
question then is: What effect has trauma under surgical
anesthesia upon the part of the brain
that remains awake?
If, in surgical anesthesia, the traumatic impulses cause an
excitation of the wide-awake cells, are the remainder of the
cells of the brain, despite anesthesia, affected in any way?
If so, they are prevented by the anesthesia from expressing
that influence in conscious perception or in muscular action.
Whether the
anesthetized cells are influenced or not must
be
determined by noting the physiologic functions of the body
after anesthesia has worn off, and in animals by an examination
of the brain-cells as well. It has long been known that
the vasomotor, the cardiac, and the respiratory centers discharge
energy in response to traumatic stimuli applied to
various sensitive regions of the body during surgical anesthesia.
If the trauma be sufficient, exhaustion of the entire
brain will be observed after the effect of the anesthesia has
worn off; that is to say, despite the complete paralysis of
voluntary motion and the loss of consciousness due to ether,
the traumatic impulses that are known to reach the
awake
centers in the medulla also reach and influence every other
part of the brain. Whether or not the consequent functional
depression and the morphologic alterations seen in the
brain-cells may be due to the low blood-pressure which follows
excessive trauma is shown by the following experiments:
The circulation of animals was first rendered
static by
over-transfusion, and was controlled by a continuous
blood-pressure record on a drum, the factor of anemia being thereby
wholly excluded during the application of the trauma and
during the removal of a specimen of brain tissue for histologic
study. In each instance, morphologic changes in the cells
of all parts of the brain were found, but it required much
more trauma to produce brain-cell changes in animals whose
blood-pressure was kept at the normal level than in the
animals whose blood-pressure was allowed to take a downward
course. In the cortex and in the cerebellum, the
changes in the brain-cells were in every instance more marked
than in the medulla.
There is also strong negative
evidence that traumatic impulses are not excluded by ether anesthesia
from the part of the brain that is apparently asleep. This evidence is
as follows: If the factor of fear be excluded, and if in addition the
traumatic impulses be prevented from reaching the brain by
cocain[3] blocking, then, despite the intensity
or the duration of the trauma within the zone so blocked, there follows no
exhaustion after the effect of the anesthetic disappears, and no
morphologic changes are noted in the brain-cells.
Still further negative evidence that inhalation anesthesia
offers little or no protection to the brain-cells against trauma
is derived from the following experiment: A dog whose
spinal cord had been divided at the level of the first dorsal
segment, and which had then been kept in good condition
for two months, showed a recovery of the spinal reflexes,
such as the scratch reflex, etc. Such an animal is known as
a "spinal dog." Now, in this animal, the abdomen and
hind extremities had no direct nerve connection with the
brain. In this dog, continuous severe trauma of the abdominal
viscera and of the hind extremities lasting for four
hours was accompanied by but slight change in either the
circulation or in the respiration, and by no microscopic
alteration of the brain-cells (Fig. 1). Judging from a large
number of experiments on
normal dogs under ether, such an
amount of trauma would have caused not only complete
physiologic exhaustion of the brain, but also morphologic
alterations of all of the brain-cells and the physical destruction
of many (Fig. 2). We must, therefore, conclude that,
although ether anesthesia produces unconsciousness, it
apparently protects none of the brain-cells against
exhaustion
from the trauma of surgical operations; ether is, so to speak,
but a veneer. Under nitrous oxid anesthesia there is approximately
only one-fourth as much exhaustion as is produced
by equal trauma under ether (Fig. 3). We must conclude,
therefore, either that nitrous oxid protects the brain-cells
against trauma or that ether predisposes the brain-cells to
exhaustion as a result of trauma. With these premises let
us now inquire into the cause of this exhaustion of the brain-cells.
