1905.] Pharmacology of Indacomtine and Bikhaconitine. 477 
duration of the systole, but as an early effect, the excitability was increased, 
spontaneous contractions often appearing after perfusion by indaconitine, 
whilst no such effect had followed from the use of the simple nutrient fluid. 
The weakened and rapid beat of indaconitine is rendered slower and stronger 
when atropine solution is substituted. 
Action on Respiration.—After temporary acceleration, slowing of the 
respiratory movements accompanied by periodical wide inflation of the 
lungs, follow medium doses of indaconitine, the flank movements being more 
obviously slowed than those of the hyoid. A _ proportion of 0:0006 to 
00008 per kilogramme, whilst having such an effect, does not arrest the 
respiration, but with a proportion of, and above 0°001 per kilogramme, 
entire suspension of respiration may ensue, so that when the lethal dose is 
nearly reached, an absence of respiratory movement (obvious and registrable) 
-mnay be observed for 24 hours or more. This condition may be coincident 
with some retention of reflex in the limbs. Before the animal resumes its 
power of regaining the ventral position when placed on the back, there is 
some return of respiratory movement. 
Hyperlethal doses up to 0°0025 gramme per kilogramme will abolish 
respiration in from 30’ onward according to their extent. The last evidence 
of some activity in the respiratory mechanism is elicited by cutaneous 
stimulation, and especially by placing the frog on the dorsum. 
Action on Reflex.—Sensory depression at the periphery is somewhat less 
powerful in the reflex (brainless) frog, under the influence of indaconitine, 
than it is under aconitine when equal proportions are given. Otherwise the 
general character of the effect is similar. 
Reaction of Nerve Muscle Preparation.—These experiments were conducted 
upon brainless frogs, in some, vascular ligature being previously applied to 
one leg. The dose used was in proportion to the total weight of the frog, 
irrespective of the parts excluded from the circulation. 
Expervments.— Rana esc. with brain destroyed received 0:00200 gramme 
of indaconitine per kilogramme. In five hours, the circulation having 
completely ceased 90’ previously, the nerve stimulated at 43 cm., the muscle 
at 16, yielded contraction of the muscle. Maximal stimulation, both direct 
and indirect, gave a series of fair contractions. 
f. temporaria (brain destroyed, left vascular ligature) received the large 
proportion of 0:024 per kilogramme. In 80’ (heart arrested) minimal 
excitability, nerve 43, muscle 23 cm. 
If after poisoning by a large dose of the alkaloid, the preparation of the 
nerve be delayed for 24 hours, a great reduction in excitability is witnessed, 
and the resulting contractions to stimulation are very much diminished in 
