ACIDOSIS 345 



not cause any muscular response. And, finally, the 

 acidity may be increased to the point at which the re- 

 spiratory and circulatory centers can no longer respond, 

 and anesthetic death that is, acid ( ?) death fol- 

 lows. It should be admitted, however, that increased 

 acidity and its phenomena may be end-effects and not 

 causes of anesthesia. 



Opposed to this postulate is the fact that the in- 

 jection of sodium bicarbonate does not overcome in- 

 halation anesthesia. Possibly there may be intra- 

 cellular acidosis which is not easily overcome by 

 alkalies. How valuable this fact may be, I do not 

 know. Certain clinical phenomena are clarified, how- 

 ever, by this postulate, and support 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, or when an 

 animal is near death from any cause. 



In striking contrast to the action of inhalation anes- 

 thetics, deep narcotization with morphin and scopolamin 

 is induced slowly and the respiratory and pulse rates are 

 progressively lessened. In addition, our experiments 

 have shown that no increase in the H-ion concentration 

 of the blood is produced by morphin or by scopolamin, 

 no matter how deep the narcotization. In animals al- 

 ready 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, shock, 

 anger or fear, the administration of morphin delayed or 

 prevented entirely the neutralization of the acidity. In 



