DUODOTE
atropine and pralidoxime chloride
LOE Approaching
INTRAMUSCULAR · INJECTABLE
acetylcholine, including excess acetylcholine due to organophosphorus poisoning, at muscarinic cholinergic receptors on smooth muscle, cardiac muscle, secretory gland cells, and in peripheral autonomic ganglia and the central nervous system. Pralidoxime Pralidoxime reactivates acetylcholinesterase which has been inactivated by phosphorylation due to an organophosphorus nerve agent or insecticide. However, pralidoxime does not reactivate acetylcholinesterase inactivated by all organophosphorus nerve agents (e.g., soman). Pralidoxime cannot reactivate phosphorylated acetylcholinesterases that have undergone a further chemical reaction known as "aging." Reactivated acetylcholinesterase hydrolyzes excess acetylcholine resulting from organophosphorus poisoning to help restore impaired cholinergic neural function. Reactivation is clinically important because only a small proportion of active acetylcholinesterase is needed to maintain vital functions. poisoning by organophosphorus nerve agents