633 
and when the stimulating influence of pilocarpin was distinctly 
noticeable, every time '/, cc. of a constant atropin-solution was 
instilled by drops, at intervals of 20 seconds, until a distinet atropin- 
action revealed itself. 
We first put the gut in the vessel containing 10 mgr. of pilo- 
carpin, left it there precisely 1'/, minutes, then transposed the gut 
to a vessel that contained, beyond the 10 mgr. of pilocarpin, also 
the quantity of atropin under examination, and watched for an arrest 
(after a definite time mostly 1—1'/, minutes) of the increase of 
tonus caused by the pilocarpin. This we assumed to be the case if 
the bases of the curves were again returned to the original level, 
no matter whether the ‘oscillatory movements” of the gut were still 
greater than before or were not. The criterion used by v. LiptH DE 
JEUDE, on the contrary was, whether or no, after the administration 
of the atropin, a distinet beginning of the fall of the curve could 
be observed, in other words v. Liprn pr Jreupr watched for the 
beginning of the antagonistic action, whereas we looked for the 
condition reached after a certain lapse of time. 
Van Lipra pr Jude had established in his publication, which we 
quoted several times in this paper, that with an increase of the 
pilocarpin-dosis (up to a 500-fold) the atropin-dosis required for the 
commencement of the antagonism augments but very little (83—5-fold). 
We knew from earlier investigations that the curve, indicating the 
ratio between the concentration and the action of pilocarpin, runs 
as is shown in fig. 2. In the beginning of the curve (a to c) small 
“uostod oy} jo uono y 
Concentration of the poison. 
Fig. 2. Scheme of a Concentration-Action curve. 
differences in concentration bring about a large difference in action; 
while with the higher concentrations the action increases only very 
