TJie Pharmacology of Pyraconitine and Methylbenzaconine. 387 



to a greater extent than pyraconitine, though if asequence is de- 

 veloped it has the same general character (the auricular second beat 

 being blocked from the ventricle). 



Whilst pyraconitine stimulates the cardiac vagus both centrally and 

 within the heart (section and atropine causing acceleration), and 

 finally occasions only a limited reduction in its activity, benzaconine 

 produces but little stimulation, and ultimately suspends the vagus 

 inhibitory action. Under these conditions atropine is, of course, 

 inoperative. Both accelerate the heart in small, but slow it in large, 

 dose, and both may disorder the sequence, but vagus inhibition is 

 much more interfered with by benzaconine. Frogs poisoned by benz- 

 aconine lose the power of voluntary movement, then reflex disappears, 

 and finally the circulation is arrested; but after pyraconitine, reflex 

 outlasts the heart's action. Late spasm occurs after the latter, not 

 after the former. Whilst in lethal doses pyraconitine has no effect 

 beyond somewhat favouring fatigue and reducing excitability of motor 

 nerves, benzaconine greatly impairs their function, and in thorough 

 poisoning may suspend it entirely. 



Action of Methylbenzaconine. 



The action of methylbenzaconine may be summed up as follows : It 

 is very feeble in its toxicity when contrasted with aconitine, but is 

 somewhat stronger than benzaconine. 



Small and medium doses, whilst slowing the heart, do not cause any 

 failure in sequence, but larger doses have this effect. They act upon the 

 rhythm of the organ, involving the movement of the auricle and ven- 

 tricle whilst ultimately the sequence of the latter upon the former is 

 impaired, so that it follows only a certain proportion of the auricular 

 " leads." This block is not removed by atropine. Whilst the passage 

 of the ventricle into the diastole is at first retarded, the contractile 

 power of the myocardium is ultimately reduced by methylbenzaconine. 



The cardiac vagus is depressed in action and its inhibitory function 

 is ultimately suspended by large doses, neither section of the vagus 

 nor atropine administration relieving the slow and faulty action of the 

 organ. 



There is evidence of slight primary stimulation of reflex cord 

 centres when ligature of vessels prevents the masking of this condition 

 by the peripheral action of the poison. The subsequent impairment 

 in cord reflexes is later in occurring and of much shorter duration 

 than the action of methylbenzaconine upon intramuscular motor 

 nerves. 



In mammals the paralytic symptoms are predominant, the fall of 

 temperature is in part attributable to this cause as well as to changes 

 in the circulation. The clonic movement and salivation (observed in 



