[6] Common side effects include dry mouth, abnormally large pupils, urinary retention, constipation, and a fast heart rate.

[15] Atropine degrades slowly, typically wearing off in 7 to 14 days, so it is generally used as a therapeutic mydriatic, whereas tropicamide (a shorter-acting cholinergic antagonist) or phenylephrine (an α-adrenergic agonist) is preferred as an aid to ophthalmic examination.

[20] The lower dose of 0.01% is thus generally recommended due to fewer side effects and potential less rebound worsening when the atropine is stopped.

[citation needed] Atropine has also been used to prevent a low heart rate during intubation of children; however, the evidence does not support this use.

However, by blocking the action of acetylcholine at muscarinic receptors, atropine also serves as a treatment for poisoning by organophosphate insecticides and nerve agents, such as tabun (GA), sarin (GB), soman (GD), and VX.

Troops who are likely to be attacked with chemical weapons often carry autoinjectors with atropine and oxime, for rapid injection into the muscles of the thigh.

[medical citation needed] Atropine was added to cafeteria salt shakers in an attempt to poison the staff of Radio Free Europe during the Cold War.

[30] One proposed mechanism for atropine's paradoxical bradycardia effect at low doses involves blockade of inhibitory presynaptic muscarinic autoreceptors, thereby blocking a system that inhibits the parasympathetic response.

[medical citation needed] A common mnemonic used to describe the physiologic manifestations of atropine overdose is: "hot as a hare, blind as a bat, dry as a bone, red as a beet, and mad as a hatter".

[34] It is generally contraindicated in people with glaucoma, pyloric stenosis, or prostatic hypertrophy, except in doses ordinarily used for preanesthesia.

Noratropine (24%), atropine-N-oxide (15%), tropine (2%), and tropic acid (3%) appear to be the major metabolites, while 50% of the administered dose is excreted as apparently unchanged atropine.

In general, atropine counters the "rest and digest" activity of glands regulated by the parasympathetic nervous system, producing clinical effects such as increased heart rate and delayed gastric emptying.

ACh binds to muscarinic receptors (M2) that are found principally on cells comprising the sinoatrial (SA) and atrioventricular (AV) nodes.

By the first century A.D. Dioscorides recognized wine of mandrake as an anaesthetic for treatment of pain or sleeplessness, to be given before surgery or cautery.

[33] The use of nightshade preparations for anesthesia, often in combination with opium, persisted throughout the Roman and Islamic Empires and continued in Europe until superseded in the 19th century by modern anesthetics.

Likewise in the Renaissance, women used the juice of the berries of the nightshade Atropa belladonna to enlarge their pupils for cosmetic reasons.

[citation needed] The pharmacological study of belladonna extracts was begun by the German chemist Friedlieb Ferdinand Runge (1795–1867).

In 1831, the German pharmacist Heinrich F. G. Mein (1799-1864)[39] succeeded in preparing a pure crystalline form of the active substance, which was named atropine.

The most commonly found sources are Atropa belladonna (the deadly nightshade), Datura innoxia, D. wrightii, D. metel, and D. stramonium.

[43] The species name "belladonna" ('beautiful woman' in Italian) comes from the original use of deadly nightshade to dilate the pupils of the eyes for cosmetic effect.

Both atropine and the genus name for deadly nightshade derive from Atropos, one of the three Fates who, according to Greek mythology, chose how a person was to die.