21 
Another mouse of this series also recovered from 0.01 milligram 
per gram body weight of nitroprussiate of soda. Of the control mice 
which had received oats soaked in water, one died from 0.015 milli- 
gram of nitroprussiate of soda, another from 0.01, while a tliird recov- 
ered from 0.008 milligram per gram. Mice which had received the 
same amount of alcohol for the same period showed an increased sus- 
ceptibility to acetonitrile. 
Results similar to the above were obtained with hydrocyanic acid; 
sodium sulphocyanate, and guanidin carbonate. 
The above results show that mice to which alcohol has been admin- 
istered for some time are distinctly more susceptible to acetonitrile 
than are those which have received no alcohol ; also that there is appa- 
rently something special about the poisonous action of alcohol, for 
certain other poisons which cause a loss of weight and so might be con- 
sidered as agents which would probably ^ dower the general resist- 
ance” do not have this effect, and finally that the increased suscepti- 
bilit}^ which the alcohol mice show toward acetonitrile seems to be a 
special case for such mice as do not show an increased susceptibility 
toward other poisons related to acetonitrile (hydrocyanic acid, nitro- 
prussiate of soda, and sodium sulphocyanate). 
It was pointed out above (p. 10) that the formation of sulphocya- 
nate from acetonitrile seemed to be a protective reaction on the part of 
the organism, the sulphocyanate being less poisonous than the hydro- 
cyanic acid formed from the nitrile. Hence it might be supposed that 
the increased susceptibility of the alcohol mice to acetonitrile is due to 
a diminution of the power of the body to convert the liberated hydro- 
cyanic acid into the sulphocyanate; in this case there should be a 
smaller excretion of sulphocyanate after nitrile in the animals on alco- 
hol than in the normal. On the other hand, the hypothesis which led 
to these experiments was that as the body, as the result of the repeated 
administration of alcohol, acquired the power of oxidizing more and 
more of the hydrocarbon residues of alcohol, it also acquired the power 
of oxidizing more and more of the methyl group of the nitrile, by 
which process more and more of the cyanogen would be set free. The 
cyanogen thus formed might or might not combine with sulphur to 
form sulphocyanate. If the former occurred, the lack of an increased 
excretion of sulphocyanate in the urine would not necessarily mean 
that there had not been increased decomposition of the nitrile. On 
the other hand, if the alcohol animal excreted an increased amount of 
sulphocyanate, this would be strong evidence that there had been 
increased destruction of the nitrile with an increased formation of 
cyanogen and the increased toxicity could thus be explained. 
In order to test the above hypotheses, determinations of the sulpho- 
cyanate in the urine were made after the administration of acetonitrile 
