Editor, – I would like to correct an error in the
article by Dr Wargon (Aust Prescr 2000;23:62-3).
The comment that an organophosphate insecticide 'acts
by non-reversibly blocking acetylcholine' is not
correct. These compounds act by non-reversibly
blocking the enzyme acetylcholinesterase which is
responsible for degrading acetylcholine at nerve
terminals. The effect of this enzyme inhibition is
an excess acetylcholine activity rather than any
blocking of the effects of this neurotransmitter.
Maldison (malathion) initially undergoes
bioactivation in the insect to the active compound
which, by my understanding, acts predominantly in
the insect's central nervous system.
Pyrethroids (also mentioned in the article) act on
voltage-dependent sodium channels in the nerve cell
membranes.
With some of these drugs, this results in repetitive
nerve firing and release of excess acetylcholine at
the nerve terminal. The end result with some
pyrethroids is therefore similar to that with the
organophosphates.
Excess muscarinic activity resulting from the
clinical use of reversible anticholinesterases (e.g.
neostigmine) is a common problem which is overcome
in anaesthetic practice by the concurrent
administration of an antimuscarinic drug (e.g.
atropine) that does block the action of
acetylcholine at muscarinic receptors. This is
important to prevent the severe bradycardia that
would otherwise occur.
Kerry Brandis
Director of Anaesthesia
Gold
Coast Hospital
Southport, Qld
