MECHANISM OF THE ANAPHYLACTIC SHOCK 155 



picture of the proceedings can be developed, but the work of Schultz, 

 Dale, Manwaring, Voegtlin, and Bernheim mark a most important 

 advance and clearly show the direction in which profitable research 

 may be pursued. 



Mechanism of the Anaphylactic Shock. If now we inquire into 

 the mechanism by which the anaphylactic shock is called forth, the 

 very suddenness of the onset and the lightning course of the reaction 

 suggest a cerebral origin of the symptoms in question. As a matter 

 of fact Besredka has shown that the shock, in guinea-pigs at least, 

 is particularly severe if the anaphylactic poison is injected intra- 

 cerebrally, and that it is then exceptional for an animal to escape 

 death, while with the usual intraperitoneal method nearly 75 per 

 cent, recover. Quite in accord with this view also is the observation 

 that it is possible either to suppress or to mitigate the severity of 

 the symptoms, if the animal is previously anesthetized with ether 

 or ethyl chloride, or is treated with hypnotics, such as urethane, 

 paraldehyde, or chloral hydrate. 



Biedl and Kraus, on the other hand, working with dogs, came to 

 the conclusion that primary injury to the brain can probably be 

 excluded, since paralysis and respiratory disturbances were not 

 observed and the reflexes did not disappear. They could note as 

 a constant symptom, however, a marked drop in blood-pressure 

 (from 120 to 150 Hgmn. to 80, 60, and even 40), which was shown 

 to be of peripheral origin, and they are inclined to attribute prac- 

 tically all other symptoms, which have been noted during the 

 anaphylactic reaction, including the drop in temperature which is 

 seen in all cases, to this one factor. The effect of the narcotics and 

 hypnotics they explain by the assumption that these remedies 

 merely render the central nervous system less susceptible to the 

 effect of stimuli resulting from the drop of blood-pressure and the 

 consequent central anemia. 



Auer and Lewis also assume a peripheral origin of the anaphyl- 

 actic symptom complex, but regard the spasmodic contraction of 

 the smallest bronchioles which is so constantly seen in guinea-pigs 

 as the essential factor, in these animals at least. It would thus 

 appear that in different animals the mechanism may be different, 

 but the possibility must also be borne in mind that these differences 

 may be more or less accidental and not essential. This idea is 

 supported by the observation of Schultz and Jordan that the bron- 



