Nerve agents cholinergic toxicity

Conventional nerve agents, such as sarin and soman, are OP compounds of pentavalent phosphorus that are well known as threats in the context of warfare and terrorism (Sidell and Borak, 1992). These substances produce acute cholinergic toxicity and death via inhibition of acetylcholinesterase (AChE) in the central and peripheral nervous systems (Marrs et al, 1996). 

In conhast to conventional nerve agents, DN agents produce permanent neurological dysfunction in the form of OPIDN rather than cholinergic toxicity and death (Richardson, 2005). Like conventional nerve agents, DN agents are OP compounds of pentavalent phosphorus that are readily synthesized, but they are designed to inactivate... 

The acute toxicity of nerve agents is usually attributed to the excessive cholinergic stimulation caused by the above-mentioned excess of ACh, followed by subsequent over-stimulation of the cholinergic pathways and desensitization of the cholinergic peripheral and central receptor sites (Dawson, 1994). 

Pyridostigmine bromide studies have been performed in dogs, guinea pigs, monkeys, rabbits, rats, and mice. Diarrhea, salivation, tremors, and respiratory failure were seen prior to death. Side effects of the drug are related to muscarinic and nicotinic effects. Toxicity is also related to cholinergic stimulation. Effectiveness of pretreatment to reduce lethality after exposure to nerve agents (in particular, soman) is dependent on the administration of atropine and pralidoxime, postexposure. 

Symptoms of toxicity should be managed to alleviate cholinergic symptoms, with special attention to respiratory support. Atropine and pralidoxime may be needed. In a military setting, symptoms should be distinguished from nerve agent poisoning to provide proper treatment. 

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