346 Dr. Cash and Prof. Dunstan. lrharmacology of 



tion in the pharmacological action, but res alts merely in a general 

 weakening of the characteristic action of the parent alkaloid. 



Considering next the effect of removing the acetyl group from 

 aconitine, which is seen in the behaviour of benzaconine, we find that 

 the characteristic features of aconitine action are almost entirely 

 annulled. The great toxic power of aconitine has been greatly 

 reduced, so that the lethal dose of benzaconine for both cold- and 

 warm-blooded animals is relatively so considerable as to remove it 

 from the class of poisons in the ordinary acceptation of the term. 



In the action of benzaconine on the heart and circulation very 

 little trace of the effects of aconitine can be observed; whilst after 

 the administration of aconitine the ventricles ultimately beat more 

 rapidly than, and often independently of, the auricles, the opposite 

 is the case in the action of benzaconine. On the heart, indeed, it 

 acts to some extent as the antagonist of aconitine, causing slowing, 

 especially of the ventricles, in opposition to the great acceleration 

 produced by aconitine, so that in a certain measure it is observed 

 that benzaconine behaves as an antidote to aconitine poisoning, 

 though not so effectively as atropine. This is a point of considerable 

 practical importance when it is remembered that benzaconine occurs 

 to a variable extent with aconine in A. napellus, from which plant 

 the ordinary medicinal preparations are made. 



The removal of the acetyl group has also abolished the stimulat- 

 ing effect of aconitine on the respiratory centres and the pulmonary 

 vagus. On the other hand, in its general action on the respiration 

 and on temperature a certain resemblance is traceable between the 

 depressant action of benzaconine and aconitine. Peripherally benz- 

 aconine depresses the activity of motor nerve endings and, in a lesser 

 degree, of skeletal muscular tissue, whilst aconitine acts principally 

 upon sensory nerve terminations. 



In contrasting the action of aconine with that of benzaconine we 

 are studying the effect of withdrawing a benzoyl group. It has 

 been seen that in removing the acetyl group from aconitine we 

 produce an alkaloid which is no longer a virulent heart poison; the 

 removal of the benzoyl or benzoic group from benzaconine furnishes 

 aconine which is so far from being a heart poison that it may be 

 ranked as a general cardiac tonic, and in virtus of this action as 

 the antagonist of aconitine. In a much greater degree than benz- 

 aconine it is an antidote to aconitine, so much so that we have 

 found that the administration of aconine is successful in averting in 

 small animals the effect of a lethal dose of aconitine. Amongst the 

 distinctive features in the pharmacological action of aconine is to be 

 noticed a curare-like effect on the motor nerve endings of the muscles 

 which is not observed with either aconitine or diacetyl-aconitine. 

 No fault of sequence between ventricles and auricles, such as is 



