ANAPHYLAXIS 365 



eludes the air passages. That the origin of this contraction is not, as 

 previously supposed, of central origin, but is referable to peripheral 

 cause, they proved by showing that the same phenomena occur in 

 the guinea pigs even after the cord and medulla have been destroyed 

 and the vagi divided. In such cases, of course, with the cord and 

 medulla destroyed, artificial respiration had to be done, and when 

 the symptoms set in it was found that the lungs could no longer be 

 expanded by the same force of artificial respiration which before this 

 had been sufficient. 



They showed also that the non-collapsible expansion of the lungs 

 after death was due to imprisonment of the air in the alveoli by the 

 contracted musculature of the small bronchioles, and further con- 

 firmed their opinion of the peripheral origin of this contraction by 

 the important discovery that atropin will markedly protect, often 

 preventing death or hastening recovery. It is noteworthy, too, that 

 Auer and Lewis speak of occasionally finding slight pulmonary 

 edema, a feature which Biedl and Kraus consider incompatible with 

 true anaphylaxis. * 



Anderson and Schultz, 14 who have (bn^rmed much of the work 

 of Auer and Lewis, find that not only atrojrin will prevent asphyx- 

 iation in these cases, but methane, chloral hydrate, adrenalin, and 

 pure oxygen will exert a similar effect. The animals may be saved 

 from suffocation in this way, but may nevertheless die, probably as 

 the result of lowered blood pressure. 



The observations of Auer and Lewis have been further confirmed 

 especially by Biedl and Kraus, 15 who regard it as well established 

 that anaphylactic death in guinea pigs is caused primarily by suffo- 

 cation, due to tetanic spasms of the musculature of the small bronchi. 

 These spasms are not of central origin, but are peripherally initiated, 

 possibly by direct action upon the smooth- muscle itself. The fact 

 that atropin is not effective in preventing death in all severe cases is 

 no argument against this, since such an eff ect^jKOuld naturally de- 

 pend upon the relation between the amount of atropin given and the 

 severity of the attack. In this connection the studies that have been 

 made upon the irritability of smooth muscle fibers in normal and in 

 sensitized animals are of great interest. Schultz, 16 following out an 

 observation made by Rosenau and Anderson, studied the intestinal 

 muscle of normal sensitized guinea pigs excised and suspended in 

 HowelPs solution. In this way he showed that during the period of 

 hypersusceptibility the smooth muscle is abnormally sensitive to 

 treatment with the antigen. The contraction which normally occurs 



14 Anderson and Schultz. Proc. Soc. Exp. Biol. and Med., 7, 1909, p. 32. 



15 Biedl und Kraus. Zeitschr. f. Immunitatsforschung, Vol. 7, 1910; 

 Centralbl f. PhysioL, 1910; Wien. klin. Woch., No. 11, 1910. 



16 Schultz. Jour. Pharm. and Exp. Therap., 1, 1910 ; 2, 1910. 



