If these premises be sound, we are justified in asserting that the state of anesthesia is due to an induced acidity of the blood. If the acidity is slight, then the anesthesia is slight and the force of the nerve impulses is lessened, but the patient is still conscious of them. As the acidity increases associative memory is lost, and the patient is said to be unconscious: the centers governing the voluntary muscles are not inhibited, however, and cutting the skin causes movements. If the acidity is further increased, there is loss of muscular tone and even the strong contact ceptor stimuli of a surgical operation do not cause any muscular response, and, finally, the acidity may be increased to the point at which the respiratory and circulatory centers can no longer respond by increased effort, and anesthetic death-- that is, ACID death--follows. Certain clinical phenomena are clarified by this theory and serve to substantiate it. For example, it is well known that inhalation anesthesia precipitates the impending acidosis which results from starvation, from extreme Graves' disease, from great exhaustion, from surgical shock, and from hemorrhage, and which is present when death from any cause is imminent. We see, therefore, that anesthesia is made possible, first, by the fact that inhalation anesthetics cause acidity, and, second, by the antithetic adaptation of the higher centers in the brain and of the centers governing respiration and circulation. In deep contrast to the action of inhalation anesthetics is that of narcotics. Deep narcotization with morphin and scopolamin is induced slowly; the respiratory and pulse-rate are progressively lessened-- and there is no acidity. By our researches we have established in what consists the generic difference between inhalation anesthetics and narcotics. In our experiments no increase in the H-ion concentration was produced by morphin or by scopolamin, no matter how deep the narcotization. In animals already narcotized by morphin the production of acid by any of the acid-producing stimuli was delayed or prevented. On the other hand, in animals in which an acidity had already been produced by ether, by shock, by anger, or by fear, the later administration of morphin delayed or inhibited entirely the neutralization of the acidity. In other words, morphin interferes with the normal mechanism by which acidity is neutralized possibly because its inhibiting action on the respiratory center is sufficient to overcome the stimulating action of acidity on that center, for, as we have stated, the neutralization of acidity is in large measure accomplished by the increased respiration induced by the acidity itself. SUMMARY