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Acetylcholinesterase: A Pretreatment Drug for Organophosphate Toxicity

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Multidisciplinary Approaches to Cholinesterase Functions

Abstract

Accumulation of acetylcholine at cholinergic receptor sites as a result of inhibition of acetylcholinesterase (AChE; EC 3.1.1.7) by organophosphorus compounds (OP) produces effects equivalent to excessive stimulation of these receptors throughout the central and peripheral nervous system.l,2 The cholinergic crisis thus produced is characterized by miosis, increased salivary and tracheobronchial secretions, bradycardia, muscle weakness, fasiculations, and convulsions, resulting in death by respiratory failure.3 The multiple drug regimen used for OP poisoning consists of pretreatment with a reversible ChE inhibitor, pyridostigmine bromide, and treatment with a combination of atropine, to counteract the effect of accumulated acetylcholine, and pralidoxime chloride (2—PAM), to reactivate inhibited AChE.4 This drug regimen is very effective in protecting experimental animals against death by OP poisoning. However, it is ineffective in protecting against performance deficits, convulsions, or permanent brain damage.4–7 An anticonvulsant drug, diazepam, was recently included as a treatment to minimize convulsions and risk of permanent brain damage.8,9

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Doctor, B.P. et al. (1992). Acetylcholinesterase: A Pretreatment Drug for Organophosphate Toxicity. In: Shafferman, A., Velan, B. (eds) Multidisciplinary Approaches to Cholinesterase Functions. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3046-6_36

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  • DOI: https://doi.org/10.1007/978-1-4615-3046-6_36

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-6328-6

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