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Systematic (IUPAC) name
(8-methyl-8-azabicyclo[3.2.1]oct-3-yl) 3-hydroxy-2-phenylpropanoate
CAS number 51-55-8
ATC code A03BA01 S01FA01
PubChem 174174
DrugBank APRD00807
Chemical data
Formula C17H23NO3 
Mol. mass 289.369
Pharmacokinetic data
Bioavailability 25%
Metabolism 50% hydrolysed to tropine and tropic acid
Half life 2 hours
Excretion 50% excreted unchanged in urine
Therapeutic considerations
Pregnancy cat.


Legal status

Rx only

Routes Oral, IV, rectal

Atropine is a tropane alkaloid extracted from the deadly nightshade (Atropa belladonna) and other plants of the family Solanaceae. It is a secondary metabolite of these plants and serves as a drug with a wide variety of effects. It is a competitive antagonist for the muscarinic acetylcholine receptor. Being potentially deadly, it derives its name from Atropos, one of the three Fates who, according to Greek mythology, chose how a person was to die.


Physiological effects and uses

Generally, atropine lowers the "rest and digest" activity of all muscles and glands regulated by the parasympathetic nervous system. This occurs because atropine is a competitive antagonist of the muscarinic acetylcholine receptors. (Acetylcholine is the main neurotransmitter used by the parasympathetic nervous system.) Therefore, it may cause swallowing difficulties and reduced secretions.

Ophthalmic use

Topical atropine is used as a cycloplegic, to temporarily paralyze the accommodation reflex; and as a mydriatic, to dilate the pupils. Atropine degrades slowly, typically wearing off in 2 to 3 days, so tropicamide (a shorter-acting cholinergic antagonist) or phenylephrine (an α-adrenergic agonist) are generally preferred as mydriatics. The effects of atropine can last up to two weeks. Atropine induces mydriasis by blocking contraction of the circular pupillary sphincter muscle, which is normally stimulated by acetylcholine release, thereby allowing the radial pupillary dilator muscle to contract and dilate the pupil. Atropine is contraindicated in patients predisposed to narrow angle glaucoma.

Atropine can be given to patients who have direct globe trauma.


Injections of atropine are used in the treatment of bradycardia (an extremely low heart rate), asystole and pulseless electrical activity (PEA) in cardiac arrest. This works because the main action of the vagus nerve of the parasympathetic system on the heart is to slow it down. Atropine blocks that action and therefore may speed up the heart rate. The usual dose of atropine is 0.5 to 1 mg every three to five minutes, up to a maximum dose of 3 mg.

Atropine is also useful in treating first degree heart block, second degree heart block Mobitz Type 1 (Wenckebach block), and also third degree heart block with a high Purkinje or AV-nodal escape rhythm. It is usually not effective in second degree heart block Mobitz type 2, and in third degree heart block with a low Purkinje or ventricular escape rhythm. Atropine is contraindicated in ischemia-induced conduction block, because the drug increases oxygen demand of the AV nodal tissue, thereby aggravating ischemia and the resulting heart block.

One of the main actions of the parasympathetic nervous system is to stimulate the M2 muscarinic receptor in the heart, but atropine inhibits this action.

Secretions and bronchoconstriction

Atropine's actions on the parasympathetic nervous system inhibits salivary, sweat, and mucus glands. This can be useful in treating Hyperhidrosis and can prevent the death rattle of dying patients. Even though it has not been officially indicated for either of these purposes by the FDA, it has been used by physicians for these purposes. [1]

Antidote for organophosphate poisoning

By blocking the action of acetylcholine at muscarinic receptors, atropine also serves as an antidote for poisoning by organophosphate insecticides and nerve gases. Troops who are likely to be attacked with chemical weapons often carry autoinjectors with atropine and obidoxime which can be quickly injected into the thigh. However, inhalation of extremely toxic agents may require a direct injection into the heart. Atropine is often used in conjunction with Pralidoxime chloride.

Atropine is given as an antidote to SLUDGE (Salivation, Lacrimation, Urination, Diaphoresis, Gastrointestinal motility, Emesis) symptoms caused by organophosphate poisoning.

Some of the nerve gases attack and destroy acetylcholinesterase, so the action of acetylcholine becomes prolonged. Therefore, atropine can be used to reduce the effect of acetylcholine.

Side effects and overdose

Adverse reactions to atropine include ventricular fibrillation, supraventricular or ventricular tachycardia, dizziness, nausea, blurred vision, loss of balance, dilated pupils, photophobia, and possibly, notably in the elderly, extreme confusion, hallucinations, and excitation. These latter effects are due to the fact that atropine is able to cross the blood-brain barrier. Because of the hallucinogenic properties, some have used the drug recreationally, though this is very dangerous and often unpleasant.

In overdoses, atropine is poisonous. Atropine is sometimes added to other potentially addictive drugs, particularly anti-diahorrea opioid drugs such as diphenoxylate or difenoxin where the secretion-reducing effects of the atropine can also aid the anti-diahorrea effects. This is supposed to prevent abuse of these drugs, however while the unpleasant side effects produced by the atropine may discourage abuse they certainly do not prevent it entirely,[2] and these combination products can be significantly more dangerous than if the opioid was administered by itself.[3]

Although atropine treats bradycardia (slow heart rate) in emergency settings, it can cause heart rate slowing when given at very low doses, presumably as a result of a weak partial agonist effect at the cardiac muscarinic receptors.[citation needed]

The antidote to atropine is physostigmine or pilocarpine.

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".[4] This set of symptoms is known as anticholinergic toxidrome, and may also be caused by other drugs with anticholinergic effects, such as diphenhydramine, phenothiazine antipsychotics and benztropine.[5]

Chemistry and pharmacology

Atropine is a racemic mixture of D-hyoscyamine and L-hyoscyamine, with most of its physiological effects due to L-hyoscyamine. Its pharmacological effects are due to binding to muscarinic acetylcholine receptors. It is an antimuscarinic agent.

The most common atropine compound used in medicine is atropine sulfate (C17H23NO3)2·H2SO4·H2O, the full chemical name is 1α H, 5α H-Tropan-3-α ol (±)-tropate(ester), sulfate monohydrate.


Mandragora (mandrake) was described by Theophrastus in the fourth century B.C. for treatment of wounds, gout, and sleeplessness, and as a love potion. By the first century A.D. Dioscorides recognized wine of mandrake as an anaesthetic for treatment of pain or sleeplessness, to be given prior to surgery or cautery.[4] The use of Solanaceae containing tropane alkaloids for anesthesia, often in combination with opium, persisted throughout the Roman and Islamic Empires and continued in Europe until superseded by the use of ether, chloroform, and other modern anesthetics.

Atropine extracts from the Egyptian henbane were used by Cleopatra in the last century B.C. to dilate her pupils, in the hope that she would appear more alluring. In the Renaissance, women used the juice of the berries of Atropa belladonna to enlarge the pupils of their eyes, for cosmetic reasons; "bella donna" is Italian for "beautiful lady".

The mydriatic effects of atropine were studied among others by the German chemist Friedrich Ferdinand Runge (1795–1867). In 1831 the pharmacist Mein succeeded the pure crystalline isolation of atropine. The substance was first synthesized by German chemist Richard Willstätter in 1901.

Natural sources

Atropine is found in many members of the Solanaceae family. The most commonly found sources are Atropa belladonna, Datura inoxia, D. metel, and D. stramonium. Other sources include members of the Brugmansia and Hyoscyamus genera. The Nicotiana genus (including the tobacco plant, N. tabacum) is also found in the Solanaceae family, but these plants do not contain atropine or other tropane alkaloids.

See also


  1. ^
  2. ^ Rao R, Agrawal A, Pal HR, Mohan I. Lomotil dependence: a note of caution. National Medical Journal of India. 2005 Nov-Dec;18(6):330-1.
  3. ^ Thomas TJ, Pauze D, Love JN. Are one or two dangerous? Diphenoxylate-atropine exposure in toddlers. Journal of Emergency Medicine. 2007 Aug 29.
  4. ^ a b Robert S. Holzman, MD (1998-07). The Legacy of Atropos 241-249. Retrieved on 2007-05-21. citing J. Arena, Poisoning: Toxicology-Symptoms-Treatments, 3rd edition. Springfield, Charles C. Thomas, 1974, p 345
  5. ^ Szajewski J (1995). Acute anticholinergic syndrome. IPCS Intox Databank. Retrieved on 2007-05-22.
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Atropine". A list of authors is available in Wikipedia.
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