Poisoning with organophosphorus insecticides.
Because of an increasing incidence of poisoning with the newer organophosphorus anticholinesterase insecticides, these compounds have been reviewed in terms of their history and pharmacology, relationship with other drugs, factors affecting toxicity, mechanism of action, toxic signs and treatment. The modern organophosphorus pesticide requires metabolic conversion before toxicity develops. Insects have a greater propensity for this conversion than humans. Nevertheless, this conversion does occur in humans and can be potentiated by other drugs. Toxicity also varies with age, sex, route and frequency of administration, and previous exposure. The mechanism of toxicity is inhibition of acetylcholinesterase, causing an intoxicating build-up of acetylcholine. Signs and symptoms consist of the clinical manifestations of unopposed parasympathetic and central activity. Treatment must be initiated early. Respiration must be maintained and the effects of acetylcholine must be counteracted by massive doses of atropine. Metaraminol enhances the antagonistic action of atropine against acetylcholine and may also be given. Once acetylcholinesterase is inactivated, restoration is slow. Recovery can be accelerated by enzyme reactivators like the oxime compounds. Pyridine aldoxime (Pralidoxime, Protopam, P(2)S and 2-PAM) can be given in combination with atropine and metaraminol (AMP therapy) and may be the treatment of choice.
D000109:Acetylcholine / Q000378:metabolism*; D001285:Atropine / Q000627:therapeutic use*; D002800:Cholinesterase Inhibitors / Q000506:poisoning*; D006801:Humans; D007306:Insecticides / Q000506:poisoning*; D008680:Metaraminol / Q000627:therapeutic use*; D010278:Parathion / Q000506:poisoning*; D011220:Pralidoxime Compounds / Q000627:therapeutic use*
D002800:Cholinesterase Inhibitors; D007306:Insecticides; D011220:Pralidoxime Compounds; D010278:Parathion; D001285:Atropine; D008680:Metaraminol; D000109:Acetylcholine
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