Nicotinic antagonists and nerve gas poisoning

White, Stuart M.; Palfreman, T M

doi:10.1258/jrsm.98.7.336-a

Cited by 1 publication

(1 citation statement)

References 3 publications

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“…Because acute OP pesticide poisoning leads to fasciculations and progressive weakness with overstimulation of these receptors, the development of competitive antagonists of neuromuscular nAChR is a logical approach to mitigating the effects of OP pesticides and their nAChR agonism. Pharmacologic protection of the NMJ with nicotinic ACh receptor antagonists has only recently been theorized …”

Section: Nicotinic Receptor Antagonistsmentioning

confidence: 99%

Pharmacotherapy to protect the neuromuscular junction after acute organophosphorus pesticide poisoning

Bird

Krajacic

Sawamoto

et al. 2016

Annals of the New York Academy of Sciences

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Organophosphorus (OP) pesticide poisoning is a leading cause of morbidity and mortality in the developing world, affecting an estimated three million people annually. Much of the morbidity is directly related to muscle weakness, which develops 1-4 days after poisoning. This muscle weakness, termed the intermediate syndrome (IMS), leads to respiratory, bulbar, and proximal limb weakness and frequently necessitates the use of mechanical ventilation. While not entirely understood, the IMS is most likely due to persistently elevated acetylcholine (ACh), which activates nicotinic ACh receptors at the neuromuscular junction (NMJ). Thus, the NMJ is potentially a target-rich area for the development of new therapies for acute OP poisoning. In this manuscript, we discuss what is known about the IMS and studies investigating the use of nicotinic ACh receptor antagonists to prevent or mitigate NMJ dysfunction after acute OP poisoning.

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Section: Nicotinic Receptor Antagonistsmentioning

confidence: 99%