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Muscarinic effects nerve agents

In addition to battlefield trauma, there is also the risk of exposure to chemical weapons such as the nerve agents, notably the organophosphorus gases (soman, sarin, VX, tabun) [6]. Organophosphorus toxicity arises largely from their ability to irreversibly inhibit acetyl-cholinesterases, leading to effects associated with peripheral acetyl-choline accumulation (muscarinic syndrome) such as meiosis, profuse sweating, bradychardia, bronchioconstriction, hypotension, and diarrhoea. Central nervous system effects include anxiety, restlessness, confusion, ataxia, tremors. [Pg.118]

AH of the nerve agents under consideration are anticholinesterase compounds and induce accumulation of the neurotransmitter acetylcholine (ACh) at neural synapses and neuromuscular junctions by phosphorylating acetylcholinesterase (AChE). Depending on the route of exposure and amount absorbed, the PNS and/or CNS can be affected and muscarinic and/or nicotinic receptors may be stimulated. Interaction with other esterases may also occur, and direct effects to the nervous system have been observed. [Pg.44]

Anticholinesterase effects of nerve agent exposure can be characterized as muscarinic, nicotinic, or CNS. Muscarinic effects occur in the parasympathetic system and, depending on the amount absorbed, can be expressed as conjunctival congestion, miosis, ciliary spasm, nasal discharge, increased bronchial secretion, bronchoconstriction, anorexia, emesis, abdominal cramps, sweating, diarrhea, salivation, bradycardia, and hypotension. Nicotinic effects are those that... [Pg.47]

Nerve agents are OP compounds, which irreversibly inhibit AChE, leading to ACh accumulation, and cause over-stimulation of muscarinic and nicotinic ACh receptors. The effect at the SA node, the primary heart control site, is inhibitory and bradycardia results. VX primarily affects neurotransmitter receptors, those of norepinephrine, and also affects the central nervous system (CNS) not related to AChE inhibition. [Pg.498]

Enzymatic hydrolysis is a primary route for elimination of nerve agents. Specifically, treatment for OP intoxication includes atropine, a muscarinic receptor antagonist, an anticonvulsant such as diazepam, and a cholinesterase reactivator, an oxime. It has been found that drag-induced inhibition of ACh release and accumulation in the synaptic cleft, such as adenosine receptor antagonist early in the OP intoxication, improves the chances of survival. Some AChE reactivators, such as bispyridinum oximes, HI 6 and HLo 7 with atropine, are quite effective. [Pg.501]

Atropine is an antidotal treatment. It is used to reverse the muscarinic signs, but it will not reverse the nicotinic effects (muscular weakness, diaphragmatic weakness, etc.). Atropine blocks the effects of accumulated acetylcholine (ACh) at the synapse and should be continued until the nerve agent is metabohzed (Midthng et al, 1985). Over-atropinization can cause hyperthermia, tachycardia, agitation, mydriasis, and ileus, which can be life threatening in the horse (Meerstadt, 1982). [Pg.729]

Although our military experience managing toxicity from nerve agent exposure is limited, exposures to related chemicals such as the OP class occur commonly each year in the USA. In 2006, there were a total of approximately 5,400 OP exposures across the USA (Bronstein et al, 2007). OPs, such as malathion, are commonly used as pesticides. OP toxicity manifests in a similar fashion as toxicity from nerve agents however, this chemical class is considerably less toxic. One case series of 16 children who experienced poisonings with OPs confirmed that pediatric patients present with toxicity differently than adults (Lifshitz et al, 1999). These children often did not manifest the classic muscarinic effects (such as salivary secretions and diarrhea) seen in adults. [Pg.926]

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. [Pg.2165]

Acute side effects occur from therapeutic doses in 1 % of patients. However, an excessive dose of an anticholinesterase drug results in a cholinergic crisis. The condition results from stimulation of muscarinic receptors and depolarization of the motor end plate. Symptoms of salivation, lacrimation, diaphoresis, weakness, and respiratory failure may result. Therapeutic use of pyridostigmine should be discontinued in the presence of nerve agent poisoning, as it may exacerbate symptoms in certain exposures. [Pg.2166]

Toxic effects occur within seconds to 5 min of nerve agent vapor or aerosol inhalation. The muscarinic effects include ocular (miosis, conjunctival congestion, ciliary spasm), nasal discharge, respiratory (bronchoconstriction and increased bronchial secretion), gastrointestinal (anorexia, vomiting, abdominal cramps, and diarrhea), sweating, salivation, and cardiovascular (bradycardia and hypotension) effects. The nicotinic effects include muscular fa-sciculation and paralysis. CNS effects can include ataxia, confusion, loss of reflexes, slurred speech, coma, and paralysis. [Pg.2351]


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