21 
Nitroprussiate of soda No effect. 
Ox gall .No effect. 
Phenol No effect. 
Picrotoxin No effect. 
Sodium arsenate No effect. 
Sodium oxalate No effect. 
Strychnine No effect . 
Trimethylenecyanide Resistance increased . 
The poisons to which the resistance of mice was most markedly 
altered by the feeding of thyroid were acetonitrile and morphine. 
Since the susceptibility of rats and guinea pigs to these poisons was 
also changed by the administration of thyroid, they were selected for 
comparative studies. 
The advantages of a method of this kind are that the experiments 
are quickly and easily carried out and that they admit of the detec- 
tion of smaller differences in activity than do the methods hitherto 
employed. It is not possible to state positively that the physiological 
activity determined in this manner is in all respects a true index of 
the therapeutic efficiency of the thyroid, but there are many reasons 
for believing this to be the case. In the first place, thyroid is pre- 
eminently a drug that influences metabolism, and the changes in the 
resistance of animals to the poisons here considered depend upon 
deep-seated, although little understood, changes in metabolism. In 
the second place, the results obtained are in complete accord with 
those observed in clinical studies and with those obtained by other 
physiological methods. In any case there seems to be much reason 
for supposing that these reactions are as true an index of the real 
physiological activity of thyroid as is its effect upon the excretion of 
urea or upon the circulation. 
The experiments were performed upon mice, rats, and guinea pigs. 
The thyroid was fed to guinea pigs in the form of tablets; to mice 
and rats in the form of cakes, according to Ehrlich’s method. Each 
cake weighed about 4 grams; mice ate about one cake, rats from one 
and a half to three cakes per day. The poisons were dissolved in 
water and injected subcutaneously. 
i. EXPERIMENTS WITH ACETONITRILE. 
Acetonitrile or methylcyanide, CH 3 CN, seems to produce toxic 
effects chiefly, if not entirely, through the slow liberation in the body 
of hydrocyanic acid. The views as to the manner in which this 
formation of hydrocyanic acid takes place have been discussed in a 
previous bulletin from this laboratory . a An additional argument for 
the view that the toxic effects of acetonitrile are due to the formation 
a Bulletin 33: Studies in Experimental Alcoholism, 1907, p. 9. 
