The vagus center is stimulated, but any effect from this is soon prevented by depression of the vagus nerve-endings, so that from large doses there regularly results a faster and somewhat stronger heart-beat. In the mammal no direct action upon the muscle is distinguished, though in the frog a dose of atropine will temporarily revive an exhausted heart. The largest dose ordinarily employed for humans hypodermatically is fa grain (0.0012 gm.); its effect on the vagus is seen in about twenty minutes, and lasts less than one hour. (See Fig. 49.) This vagus effect shows both at the sinus node and at the auriculo-ventricular node. Atropine is thus able to check a heart-block brought about by digitalis, and to annul the valuable action of digitalis in auricular fibrillation. In one case (Laslett) of standstill of the whole heart with pauses of five to eight seconds, atropine restored the normal rhythm by cutting off the vagus effect on the sinus node.


The vasoconstrictor center is slightly stimulated, and this, with the increased rate of the heart, causes a rise in arterial pressure. This is easily demonstrated in a dog. The contraction of the arteries is most marked in the splanchnic area. In man, however, the rise in blood-pressure from even maximal therapeutic doses is usually inappreciable, and if present is entirely due to the increased heart-rate (Sollmann and Pilcher). Berezin found no effect on the pulmonary vessels. In poisoning the vasoconstrictor center tends to be depressed.

The Cutaneous Arterioles

From poisonous amounts the arteries of the skin, especially those of the head and neck, are dilated; and a flushed face or an erythematous rash like that of scarlet fever is characteristic of atropine poisoning. The flushed skin is from a central action, as there is no flushing if the sympathetic in the neck is divided.

The Blood

It has been stated that the eosinophiles are increased in number, but Herrick found this not to be the case in the guinea-pig.


A large dose of atropine is followed by deeper and more rapid breathng and a considerable increase in the amount of air inspired. This is largely due to stimulation of the respiratory center. There is probably also depression of the motor endings of the vagus, resulting in dilatation of the bronchi, and depression of the sensory ends of the vagi in the bronchi, for stimuli through these usually slow respiration. In a number of cases the author failed to obtain a change in the rate of respiration from hypodermatic injections of -fa and fa grain (1-1.3 mg.). Edsall and Means by doses large enough to cause marked increase in pulse-rate were unable to affect the breathing in Cheyne-Stokes respiration due to cerebral hemorrhage; but in a normal human obtained decided stimulation from a dose that produced toxic symptoms. Higgins and Means go so far as to say that any effect on the respiration is due to dilatation of the bronchi and increased metabolism.

The drug is much used in narcotic poisoning, especially that from morphine. Vollmer (1892) reported that a dog inspiring 4500 c.c. of air per minute was given 1 grain (0.06 gm.) of morphine sulphate at 8.45. At 3.40 the air inspiration was 4000 c.c. Then 1/20 grain (0.003 gm.) of atropine was given, and in fourteen minutes the inspiration was 6000 c.c; in twenty-one minutes, 10,000 c.c. But excessive doses exhaust the center, and must be guarded against in the use of the drug as an antidote. Exhaustion of the center is the cause of death.

The secretions of nose, throat, and bronchi are diminished, so that the membranes are dry and the mucus thick and tenacious. Excessive contraction of the bronchial muscles, as in spasmodic asthma, is overcome by depression of the bronchomotor vagal nerve-endings.


The effect from therapeutic doses is very little, but after poisonous amounts there is psychic stimulation, and the patient becomes talkative and wakeful, without any pronounced intellectual stimulation like that from caffeine. The poisoning may go on to a delirium, usually of cheerful, loquacious type, and may even result in maniacal excitement. Cerebral depression does not generally ensue until the centers have become exhausted, and then there may follow mental confusion and narcosis leading to sleep, stupor, and coma. In therapeutic amounts the drug is not a narcotic.

The motor areas are also stimulated by poisonous doses, as shown by the increased response to electric stimulation of the exposed brain and by the restless activity. The general exhilaration observed after overdoses is known as the "belladonna jag," but though it superficially resembles that from alcohol, it is true stimulation, as shown by the increased excitability of the motor areas and the larger doses of narcotic necessary to depress the intellectual powers.

The medulla, after large hypodermatic doses, shows stimulation of the respiratory center, with weak stimulation of vagus and vasoconstrictor. Death takes place from exhaustion and paralysis of the respiratory center.

The spinal cord is stimulated by large doses, the increase in reflex excitability being manifested by twitching of the muscles. In the late stages of poisoning twitching may also result from asphyxia.

The peripheral nerves have already been spoken of.

Comparing atropine with caffeine and strychnine as central stimulants, we might say that, in therapeutic doses, all three stimulate the medullary centers, and of these chiefly the respiratory; but that caffeine, in addition, stimulates the intellectual functions, and strychnine the spinal or reflex functions. 26