212 WARFIELD T. LONGCOPE AND GEORGE M. MACKENZIE 



follows : (1) The amount of urea formation in both normal and sensitized 

 animals corresponds to the weight of the animal. Urea formation was 

 found to continue, under the conditions of the experiment, for at least 

 an hour and a half after excision. (2) Normal livers, upon the addition 

 of serum, showed no diminution of urea formation. (3) Livers of anaphy- 

 lactic pigs, however, while showing normal urea formation hefore the 

 antigen was added to the perfusion fluid, appeared to lose completely the 

 power of urea synthesis, when the antigen was added. (4) If the serum 

 was added drop by drop so as to produce anti-anaphylaxis, no inhibition 

 of urea-synthesis occurred. 



An investigation of the nitrogen of the blood in anaphylaxis and pep- 

 tone poisoning reported recently by Hisanobu fails to confirm Rumpf's 

 results unless we assume -that the increase of blood urea in serum anaphy- 

 laxis, reported by Hisanobu, is due to extrahepatic urea synthesis. Be- 

 sides an increase of blood urea, Hisanobu also found that there was a 

 rise during anaphylactic shock of the total non-protein nitrogen, the "rest" 

 nitrogen and the amino nitrogen. Figures for all these substances in 

 peptone shock were intermediate between those found in control pigs and 

 pigs with serum anaphylaxis. This is in agreement with results obtained 

 by Whipple and Van Slyke(&) in studying the effect of proteose intoxica- 

 tion upon the nitrogenous products of the blood. We shall refer later to 

 the effects of peptone injections on metabolism in connection with a 

 discussion of the alteration of temperature regulation caused by anaphylac- 

 tic reactions. It is pertinent, however, to recall here the fact that Mendel 

 and Rockwood had already shown that parenteral introduction of edestin 

 was followed by increased nitrogen elimination in excess of the amount of 

 nitrogen injected. 



It can scarcely be doubted that the reaction of a sensitized animal to 

 reinjection of the specific antigen entails significant changes in protein 

 metabolism, but at the present time the evidence is so conflicting and so 

 many phases of the problem are still uninvestigated that any compre- 

 hensive statement concerning nitrogen metabolism in anaphylaxis is 

 impossible. The weight of evidence points to an increase of the end 

 products of protein metabolism in both the urine and circulation and 

 therefore supports the assumption that the anaphylactic reaction is as- 

 sociated with an increase in protein katabolism. It seems probable also 

 that with this quantitative change, there also is a qualitative alteration 

 in protein metabolism, so that during anaphylactic reactions, nitrogenous 

 substances not normally formed are elaborated. 



Respiratory Metabolism. The question of gas exchange in the ana- 

 phylactic reaction was first studied in England by Scott and in Ger- 

 many by Loening. The former found that with an experimental error of 5 

 per cent, the output of CO 2 fell 35 per cent in animals subjected to passive 

 anaphylactic shock. In active anaphylaxis, when the symptoms were slight 



