SOME ASPECTS OF ANAPHYLAXIS 439 



total loss of direct irritability to mechanical and electrical stimuli; the 

 lungs show areas of emphysema, but collapse more or less completely 

 when the thorax is opened ; the blood shows delayed coagulability, but by 

 no means as great as that observed in a dog. The fall in blood pres- 

 sure is probably secondary to the failure of the heart. In the guinea- 

 pig, the lungs are the chief organs affected and their function is abol- 

 ished by a stenosis of the finer air passages preventing in the final stage 

 both the entrance and exit of air, so that death results from asphyxia. 

 The anatomical sign of this condition is furnished by the large inflated 

 lungs which do not collapse on excision from the chest cavity (Fig. 1). 

 The heart keeps on beating after final respiratory stoppage, with no 

 obvious loss of irritability; the blood shows only a slight delay in 

 coagulation and the fall in blood pressure is probably due to the fatal 

 asphyxia. These differences between the three species of animals show 

 clearly the necessity of judging each species by the anaphylactic signs 

 characteristic for it and not by manifestations only found in another 

 species. This important point, that each animal species must be meas- 

 ured by its own yard-stick when examined in anaphylaxis, has not been 

 realized, unfortunately, by some investigators. 



Causation of Anaphylaxis. — The remarkable phenomena which char- 

 acterize anaphylaxis early led investigators to search for the causative 

 agent. Numerous theories, more or less supported by experimental 

 facts, were advanced to explain how, for example, the originally harm- 

 less horse serum becomes toxic when injected into an animal sensitized 

 by this substance. The pioneer work of Vaughan, Friedemann and 

 Friedberger deals particularly with this aspect of anaphylaxis. A dis- 

 cussion of all the theories here, however, would lead too far and would 

 only befog the reader. It will suffice to state that the basic idea of the 

 chief theory is that the sensitized organism has acquired the power to 

 split the alien serum very rapidly into its components when injected 

 for the second time, and that these components then act as a poison. 

 There can be no theoretical objection to this conception; it is a legiti- 

 mate working hypothesis. But there are weighty objections just as 

 soon as one substance or mixture of substance is produced from pro- 

 teids in the test tube by chemical or biological processes and considered 

 as the causative agents of anaphylaxis because when injected into nor- 

 mal animals they produce more or less completely the signs and symp- 

 toms which are characteristic of true anaphylaxis. The assumption 

 may be true, but no rigid proof has so far been advanced that these 

 substances really are produced in the animal body during anaphylaxis. 

 The mere fact that these toxic substances produce a lesion which also 

 occurs in true anaphylaxis, by no means justifies the conclusion that 

 the causative agents were the same in the two processes. Take, for 

 example, the pale, rigid, distended lungs produced in a sensitized guinea- 



