. 214 WARFIELD T. LONGCOPE AND GEORGE M. MACKENZIE 



In both the normal and hypersensitive animal the dose can be so graded 

 as to produce either a rise or a fall in temperature, and between the two, 

 a dose can be found which produces no temperature change. But between 

 the normal and hypersensitive animal there is a striking quantitative 

 difference. In guinea-pigs, for example, the hypersensitive animal shows 

 the temperature reaction after 1-500,000 to 1-1,000,000 of the dose pro- 

 ducing the same type of temperature reaction ' in the normal animal. 

 Schittenhelm, Weichardt and Hartmann and Leschke cited experi- 

 ments confirming with rabbits and dogs these observations made on guinea- 

 pigs. Of considerable interest in this connection is the work of Friedmann 

 and Davidson on the temperature reactions following injections of sodium 

 chlorld. Using a 0.75 per cent NaCI solution, they found that rabbits 

 in the anaphylactic state reacted more sensitively, judged by the tem- 

 perature reaction, than normal animals. Normal rabbits injected sub- 

 cutaneously with 5 c.c. to 23 c.c. per kilo showed fever for a day. A 

 smaller dosage than this caused no change in temperature. Anaphylactic 

 animals, on the other hand, reacted when 2 c.c. to 5 c.c. per kilo were 

 injected. Moreover, in the anaphylactic animals, the reactions come on 

 within two to three hours after the injection, while in the normal animal 

 no temperature change is observed for six to eight hours. 



We have already referred to the experiments of Leschke on the gas 

 exchange and temperature reaction of anaphylactic animals and to his 

 conclusions that with anaphylaxis there comes a depression of the intra- 

 cellular combustion processes. If this be true, then we must assume that 

 in those reactions to reinjection in which there is a rise of temperature 

 that some additional mechanism comes into action. If less heat is being 

 produced at the time the temperature is above normal, there must be 

 some disturbance of the mechanism of heat loss. Perhaps the results of 

 Hirschfeld, who found a vasoconstrictor substance in the serum and 

 plasma of anaphylactic pigs, will prove to be of some significance in this 

 connection. Nevertheless, opposed to this are the experments of Pfeiffer 

 and Jarisch, who were able to abolish the temperature drop of anaphylactic 

 shock by administering barium chlorid, the vasoconstrictor action of 

 which presumably lessens heat -loss. Pfeiffer and Jarish concluded from 

 this barium chlorid effect that the assumption of diminished heat produc- 

 tion in anaphylactic reactions was untenable. We know from Weil's (h) 

 studies, that there is a vasomotor depression with marked engorgement of 

 the liver in canine anaphylaxis. Theoretically, therefore, it is possible to 

 explain the different temperature reactions after reinjection of hyper- 

 sensitive animals by varying degrees of participation of four factors 

 heat production, peripheral vasoconstriction, internal vasomotor depres- 

 sion, and alterations in blood-pressure. 



Serum and Cellular Ferments. One of the most, interesting phases of 

 the pathological physiology of anaphylaxis is the question of the part 



