Pralidoxime as an insignificant reactivator in severe anticholinesterase (organophosphate insecticide) poisoning.

Abstract

In acute severe anticholinesterase poisoning by organophosphate compounds, pralidoxime (P-2-AM, pyridine-2-aldoxime methiodide) used in the recommended doses, intravenously, has not been shown to reactivate the inhibited cholinesterase, as evidenced both clinically and biochemically. In vitro studies using pralidoxime iodide up to ten times the recommended concentrations, produced insignificant reactivation of cholinesterases inhibited by the organophosphate insecticide Bidrin (di-methyl-3-hydroxyl-N, N-dimethyl-crotonamide phosphate). This was even so despite prolonged exposure of the inhibited cholinesterases to the oxime. The value of pralidoxime as a reactivator of phosphorylated cholinesterases is therefore in doubt, and should not be used in preference to large doses of atropine and other supportive treatment in poisoning by organophosphate insecticides.

• Authors: A Ganendran, S Balabaskaran
• Journal: The Southeast Asian journal of tropical medicine and public health (Southeast Asian J Trop Med Public Health) Vol. 7 Issue 4 Pg. 543-50 (Dec 1976) ISSN: 0125-1562 [Print] Thailand
• PMID: 1030852 (Publication Type: Journal Article)

Chemical References

• Cholinesterase Inhibitors
• Enzyme Reactivators
• Insecticides
• Organophosphorus Compounds
• Pralidoxime Compounds
• Acetylthiocholine
• Butyrylthiocholine
• Atropine

Topics

• Acetylthiocholine
• Atropine (therapeutic use)
• Butyrylthiocholine
• Cholinesterase Inhibitors
• Dose-Response Relationship, Drug
• Enzyme Reactivators
• Humans
• Insecticides (poisoning)
• Malaysia
• Organophosphorus Compounds
• Pralidoxime Compounds (pharmacology, therapeutic use)