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Atropine is often used in conjunction with the oxime pralidoxime chloride. Some of the nerve agents attack and destroy acetylcholinesterase by phosphorylation, so the action of acetylcholine becomes excessive and prolonged. Pralidoxime (2-PAM) can be effective against organophosphate poisoning because it can re-cleave this phosphorylation.
Oximes like these do have side effects and they include liver damage, kidney damage, nausea, vomiting, but they are very efficient antidotes to nerve gas poisoning. Usually treatment of poisoning includes the use of atropine, which can slow down the action of the poison, giving more time to apply the oxime.
The health effects associated with organophosphate poisoning are a result of excess acetylcholine (ACh) present at different nerve synapses and neuromuscular junctions across the body. Specifically, acetylcholinesterase (AChE), the enzyme that normally and constantly breaks down acetylcholine, is inhibited by the organophosphate substance.
Treatment is typically with the antidotes atropine and pralidoxime. [4] Atropine, an antagonist to muscarinic acetylcholine receptors , is given to treat the physiological symptoms of poisoning. Since muscular response to acetylcholine is mediated through nicotinic acetylcholine receptors , atropine does not counteract the muscular symptoms.
As a result of cholinergic crisis, the muscles stop responding to the high synaptic levels of ACh, leading to flaccid paralysis, respiratory failure, and other signs and symptoms reminiscent of organophosphate poisoning. Other symptoms include increased sweating, salivation, bronchial secretions along with miosis (constricted pupils).
Pralidoxime (2-pyridine aldoxime methyl chloride) or 2-PAM, usually as the chloride or iodide salts, belongs to a family of compounds called oximes that bind to organophosphate-inactivated acetylcholinesterase. [1] It is used to treat organophosphate poisoning [2] in conjunction with atropine and either diazepam or midazolam. It is a white solid.
The ATNAA provides atropine and pralidoxime chloride in a single delivery system, although the two drugs are separate within the device. [1] [2] The use of the device is only to be administered in the extreme case of organophosphate poisoning.
In the 1850s, atropine was used as antispasmodic in asthma treatment and as morphine antidote for its mydriatic effect. [4] Bezold and Bloebaum showed that atropine blocked the effects of vagal stimulation on the heart in 1867. Subsequently in 1872, Heidenhain found its ability to prevent salivary secretion. [6]