Preparation. - By dissolving atropine in dilute sulphuric acid and evaporating.

Characters. - A colourless powder.

Solubility and Reactions. - Soluble in water, forming a solution which is neutral to test paper, and when applied to the eye dilates the pupil as the solution of atropine does. It leaves no ash when burned with free access of air.

Uses. - Intended for external application. It is a powerful poison.



Liquor Atropinae Sulphatis

(1 in 100 of camphor water).

Lamellae Atropinae

(1/5000 gr. in each).

U.S.P. None.

General Action of Belladonna or Atropine. - The first toxic symptoms to appear after a small dose are dryness of the mouth and headache. After full doses the pupils become dilated, a red rash appears on the skin like that of scarlatina, and a delirium of a peculiar and often of a pleasant character ensues, in which there is a great desire for movement and activity, with a feeling of great lassitude (p. 200). The pulse becomes rapid. This is generally followed by sleep.

With large doses, the mouth becomes so dry that swallowing is almost impossible, and the attempt to swallow may bring on general convulsions like hydrophobia; these convulsions are followed by paralysis, stupor, often alternating with delirium, coma and death, preceded by marked failure of the heart's action and of respiration. Death is due to asphyxia.

Special Action. - Locally applied it diminishes the sensibility of the sensory nerves (whether applied as liniment or injected subcutaneously). It can be absorbed from the skin and produce its general symptoms.

It stimulates the centres in the brain, but tends to paralyse the ends of the motor nerves, hence causing that peculiar form of delirium in which a constant desire for action is associated with lassitude. The spinal cord is first stimulated, then paralysed.

In a frog the primary stimulation quickly passes off, and there follows gradually increasing weakness both of respiratory and voluntary movements, until these become entirely abolished. If the frog be kept in this condition for four or five days, this state of absolute paralysis passes off and is succeeded by a condition of excitement with violent tetanic convulsions which may be brought on by the slightest afferent stimulus. Various explanations of this action have been given (vide p. 171).

The endings of motor nerves in voluntary muscles are paralysed by large doses, but small doses will paralyse the efferent nerve-endings which terminate in peripheral ganglia (e.g. vagus), and in involuntary muscle (p. 139). The converse is the case with curare.

Atropine has no action on voluntary muscles. Involuntary muscle is paralysed by large doses (p. 139).

On the Eye. - The pupil is dilated and the eye becomes bright, dry, and injected. The power of accommodation is paralysed, and by large doses intraocular tension is increased. For the mode of action, vide pp. 220-225.

On the Circulation. - The action of atropine on the excised heart of the frog affords an illustration of the statement I have made (p. 45), that in all probability contradictory observations frequently depend on differences in the temperature at which the observations were made. Thus Bowditch and Luciani found the contractions, both of the frog's heart containing ganglia and of the apex alone (p. 308), were rendered more powerful by atropine, while Gnauck, on the contrary, found that the contractions of the ventricle were diminished both by atropine and hyoscyamine. Kronecker and Schapiro have found that these contradictory observations are both correct, but at different temperatures. When the temperature is low (7° to 8° C.) the ventricular contractions are enlarged by atropine, but diminished by it when the temperature rises over 15° C. Large doses of atropine completely paralyse the intracardiac inhibitory apparatus, while at the same time they stimulate the vagus centres in the medulla.

Atropine is supposed to act upon inhibitory ganglia in the heart itself, not upon the vagus endings, in which respect it differs from nicotine (vide p. 314).

Sometimes there is a primary slowing of the pulse rate, followed by quickening; but it is uncertain whether this is due to stimulation of the vagus centre, or of the inhibitory apparatus in the heart.

Small doses raise the blood-pressure by stimulating the vasomotor centre in the medulla, but large doses diminish it by paralysing the vaso-motor centre and partly by paralysing the peripheral vaso-motor ganglia or muscular fibres of the walls of the arteries themselves (p. 282). Atropine also diminishes the sensibility of the heart to changes of pressure within it (p. 299).

On Respiration. - Atropine first quickens, and then slows respiration. This is due to stimulation and subsequent paralysis of the respiratory centre in the medulla. When injected into the jugular vein it appears to paralyse the ends of the sensory fibres of the vagus in the lungs, and thus tends to slow respiration at first (p. 245). It arrests secretion from the bronchial mucous membrane (p. 250).

On Secretion. - Atropine paralyses the secreting fibres of the chorda tympani without affecting the vaso-dilator fibres, so that when the chorda tympani is stimulated, either directly or reflexly, the flow of blood to the gland is increased, but no fluid exudes from the duct (p. 361).

It probably has a similar action on many, if not all, glands, including the sweat-glands, milk-glands, mucous glands, pancreas, and liver. When locally applied it stops the secretion of milk and sweat. In the case of the sweat it probably paralyses the efferent sweat-fibres which accompany the vaso-motor fibres and start from centres in the lumbar and lower dorsal parts of the cord (Luchsinger). It does not, however, prevent secretion in the intestine after division of the intestinal nerves (Brunton and Pye-Smith).

The secretion of urine is sometimes increased, but large doses may cause retention from paralysis of the bladder.