RESPIRATION 205 



an hour after the meal. This is rapidly followed by an equally 

 marked fall below normal, culminating about one and one-half 

 hours after the meal, with a subsequent rapid return to normal. 



Bennett and Dodds 53 have found that the rise of alveolar CO 2 

 just after a meal is closely related to the concentration and rate 

 of secretion of the gastric hydrochloric acid as indicated by 

 samples taken from the stomach. In cases where there is little or 

 no secretion of HC1 the rise in alveolar CO 2 is absent, though the 

 fall due to alkaline secretion into the intestine is still present. 

 Another cause of variation in alveolar CO 2 pressure is the charac- 

 ter of the diet. With an alkali-forming vegetable diet the alveolar 

 CO 2 pressure is quite considerably higher than with an acid-form- 

 ing meat diet. This was brought out very clearly in some of the 

 experiments of Hasselbalch alluded to above; and he showed at 

 the same time that the reaction of the urine varied in correspond- 

 ence with the changes in alveolar CO 2 pressure. 



During starvation the body is living on what amounts to an 

 acid-forming diet, and Higgins 54 has shown that during starva- 

 tion the alveolar CO 2 pressure falls. Perhaps the most striking 

 effects are obtained with a carbohydrate-free diet. This leads to 

 the formation within the body of a certain amount of aceto-acetic 

 and oxybutyric acids, as in severe diabetes. Higgins, Peabody, 

 and Fitz 55 showed that there is a striking fall in alveolar CO 2 

 pressure, together with a very large elimination of oxybutyric and 

 aceto-acetic acid by the kidneys, and an accompanying large in- 

 crease in ammonia excretion and excretion of acid. 



All the available evidence points, therefore, to the conclusion 

 that practically speaking the regulation of breathing in man dur- 

 ing rest under normal conditions is regulation of the blood re- 

 action. This very important conclusion is the outcome of the 

 present chapter. 



Addendum. Within the limits of the present book it is un- 

 fortunately impossible to deal in detail with the mass of quite 

 recent literature bearing on the regulation of blood alkalinity. 

 Some of this literature is based on assumptions with which, for 

 the reasons already given, I am unable to agree : while other parts 

 of it are concerned with details as to which it seems difficult for 

 the present to form definite judgments. In general, however, it 



K Bennett and Dodds, Brit. Journ. of Exper. Pathol., II, p. 58, 1921. 

 "Higgins, Publication No. 203, Carnegie Institution of Washington, p. 168, 



- 



Higgins, Peabody, and Fitz, Journ. of Med. Research, XXXIV, p. 263, 1916. 



