A little pharmacology on Atropine.

Atropine is an Anticholinergic drug. This means that it inhibits the action of acetylcholine, a neurotransmitter both in the brain and the body. It has the distinction of being the transmitter that is used in sending signals to muscles.

Because of this, Atropine is used as a remedy for nerve gas exposure. Nerve Agents usually work by destruction of the uptake mechanism for acetylcholine. This causes the muscles to spasm out of control as acetylcholine builds up in the synapses. Atropine lessens the effect so that the body can fix the problem caused by the nerve agent.

Atropine, in higher doses then those used to dilate pupils, or medicinally (to treat some heart conditions) for other purposes, can cause vivid hallucinations where the user cannot tell the difference between hallucination and reality.

The first signs of effect from atropine are dry mouth and rapid heartbeat.

To back thecarp up, this is the stuff that Nicholas Cage's character in The Rock (rather dramatically) injected into his own heart, to prevent him from succumbing to the nerve gas from the crushed plastic bubble he crushed into the mouth of the guy he was fighting.

Arguably though, all he really needed was an intravenous shot of the stuff, not an actual intracardiac shot ... but I guess he was desperate.

Atropine in the strictest sense does not an inhibit the action of acetylcholine (i.e. it does not cause any changes in the activity/structure of acetylcholine itself). It is an antagonist to acetylcholine receptors, thus competing with acetylcholine for binding sites and increases the amount of acetylcholine needed to reach Kd, as can be seen on a graded dose-response curve.

Atropine acts on only muscarinic acetylcholine receptors (turbocurare works on nicotinic acetylcholine receptors). Skeletal muscle only works through nicotinic acetylcholine receptors, so atropine would do little to stop the uncontrolled spasms associated with organoflourophosphates (nerve gas). Atropine would counteract the effects of nerve gas on smooth muscle (muscarinic receptors), but these contractions are slow and would not be spasmodic.

The primary therapeutic effect of atropine in the event of nerve gas poisoning is the prevention of heart failure. Acetylcholine acts through muscarinic receptors in the heart to slow down heart rate. Thus, addition of atropine stimulates an increase of heart rate, preventing heart failure.

Muscarinic acetylcholine receptors are pervasive throughout the body, including the GI tract, urinary tract, and sweat glands. Antagonism of these receptors by atropine causes GI malfunction (lack of GI and bladder tone causes constipation and the the inability to urinate, respectively). Inactivation of muscarinic sweat receptors causes a decreased secretion of sweat. All of these side effects make atropine therapy extremely unpleasant for the patient. Thus, atropine is unpopular as a clinical therapeutic, and is reserved for more extreme uses (such as nerve gas poisoning).

At"ro*pine (#), n. [Gr. inflexible; hence , one of the three Parcae; priv. + to turn.] Chem.

A poisonous, white, crystallizable alkaloid, extracted from the Atropa belladonna, or deadly nightshade, and the Datura Stramonium, or thorn apple. It is remarkable for its power in dilating the pupil of the eye. Called also daturine.


© Webster 1913.

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