34 Society for Experimental Biology and Medicine. 



HCN, it was found that the toxicity of the various compounds dif- 

 fered greatly. The toxicity depends in general upon the ease with 

 which the HCN is split off ; in some cases this seems to bear a 

 relation to the ease with which the residue that is united to the CN 

 group is oxidized in the body. Benzonitrile, containing the group 

 C 6 H 5 , which is oxidized with difficulty in the body, is scarcely more 

 poisonous than phenol. Acetonitrile, also containing a group, 

 CH 3 , which is oxidized with difficulty, is also but slightly toxic. 

 Propionitrile and formaldehydcyanhydrin, which contain easily 

 oxidizable groups, C 2 H 5 and CH 2 OH, are very poisonous. 



The toxicity of the molecules of a few nitriles is greater than 

 that of HCN itself, although the latter was the only toxic agent 

 involved. Thus the molecule of chloralcyanhydrin, CC1 3 CH (OH) 

 CN, is nearly twice as toxic as that of HCN. The probable ex- 

 planation of this is that the chloral residue with which the CN is 

 in combination causes the compound to be distributed especially 

 to the central nervous system ; the HCN is thus split off in 

 greater concentration in these important organs than is the case 

 after the administration of a compound which is distributed more 

 uniformly to important and unimportant organs. Through the 

 application of this principle it may be possible to modify the distri- 

 bution in the body of a remedial agent, so that the active principle 

 may be present in especially great concentration in the organs 

 which it is desired to affect. It was suggested that the power- 

 ful action of nitroglycerin upon the bloodvessels may be ex- 

 plained on a similar hypothesis. The view of Hay, that the dilation 

 of the bloodvessels caused by nitroglycerin is due to the forma- 

 tion in the body of nitrites from this substance, has been generally 

 accepted, although the objection has been made that the produc- 

 tion of a given effect requires two hundred times as much sodium 

 nitrite as nitroglycerin. This criticism may be met by the hy- 

 pothesis that the glycerin residue of the nitroglycerin causes this 

 compound to be distributed especially to the arterial walls, and 

 that the nitrite will be formed in greatest concentration at the point 

 where it exerts its action. 



The work of Heymans and Masoin on the antagonistic action 

 of sodium thiosulfate toward certain nitriles was extended to many 

 new cyanogen compounds. In addition to the thiosulfate, several 



