The action of aconite, which has lately been studied by Cash and Dunstan, is due chiefly to the aconitine in it, and therefore they may be considered together.


Applied to the skin, to a mucous membrane, or to a raw surface, aconitine and therefore aconite, first stimulates and then paralyzes the sensory nerves; it therefore causes first tingling, then numbness and local anaesthesia, which last some time. Unless the skin is sound a dangerous quantity may be absorbed. It is intensely irritant to the nostrils, causing, when it is inhaled, sneezing and much secretion with an icy cold sensation.


Gastro-intestinal tract. - Unless it is very dilute, numbness and tingling are produced in the mouth. There are no other gastro-intestinal symptoms unless the dose is very large, when there may be vomiting and purging.

Heart. - If small doses are given, the rate of the beat is soon very decidedly steadied and slowed, shortly after that the force and tension become less, and these effects are mainly due to a stimulation of the roots of the vagus. But after larger doses the pulse quickens, misses beats, and becomes irregular. Many of the ventricular beats have no corresponding auricular contraction, although the two auricles always contract together and the two ventricles contract together. As the irregularity and frequency of ventricular contractions increase, the blood-pressure rapidly undergoes great variations. It is not until quite the end of its action that aconite influences the heart muscle. The ventricles, always more affected than the auricles, pass into a condition of delirium. Even small doses lead to a fall of blood-pressure, but all the effects on blood-pressure are almost entirely secondary to the action on the heart or its nerves. The vaso-motor centre is only slightly affected. Clinically it would appear that the peripheral vessels are dilated. Aconite has been named the vegetable lancet.

Respiration. - The respiration, after a transitory quickening, is slowed, expiration and the pause after it are considerably prolonged. The movements become more slow and dyspnoeal, the respiratory centre is powerfully depressed, but it is not easy to decide whether death is due to this or to cardiac failure.

Nervous system. - It appears clear that aconite, whether given internally or applied locally, depresses the activity of the peripheral terminations of the nerves; the nerves of common sensation and temperature are affected before the motor. Any pain that may be present is relieved. Large doses in man cause clonic convulsions, chiefly respiratory. Later on, the paralysis of the motor nerves gives rise to muscular weakness. It is doubtful whether the cord is influenced. The brain is not. The pupil is dilated.

Temperature. - Aconite causes a febrile temperature to fall, This is in part due to its action on the circulation and respiration, but probably other causes are at work.

Skin. - Aconite is a mild diaphoretic; in this case also we do not understand how it acts. The cutaneous blood-vessels are generally dilated. Occasionally it produces an erythematous rash.

Kidneys. - It is said to be a feeble diuretic, but its effect is very slight, Aconitine is excreted in the urine.

Benzaconine is bitter, and does not cause tingling or numbness of mucous surfaces; in large doses it slows the pulse-beat very strikingly because the auricular beats are frequently not followed by ventricular contraction. Its action is probably chiefly on the heart muscle itself. It does not paralyze sensory nerves, but greatly interferes with motor nerves and causes a semi-comatose condition. The fall of temperature produced by it is very slight. It will be noticed that it is in almost all respects contrary in action to aconitine.

Aconine is bitter, but does not produce numbness. It is non-toxic as regards the heart, and opposes the cardiac incoordination and asequence caused by aconitine. It depresses motor nerves and respiration very strikingly, probably acting like curare.

It is worth noting that, whilst the introduction into aconitine of two additional acetyl groups (as in diacetyl-aconitine) gives rise to a derivative very similar in action to aconitine, the loss of the acetyl group, as in benzaconine, almost entirely abolishes all physiological resemblance to aconitine. On the other hand, the removal of the benzoyl radical from benzaconine (aconine remaining) produces much less alteration in action, although it does not diminish the toxicity of benzaconine.