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Antidote Treatment Nerve Agent

ATNAA antidote treatment nerve agent 50% of those exposed... [Pg.255]

Bajgar J., Fusek J., Sevelova L., Kassa, J. (2004). Original trans-dermal prophylactic antidote against nerve agents - TRANSANT. CB Medical Treatment Symposium, April 25-30, 2004, Spiez, Switzerland. Technical Program p. 14. [Pg.981]

Tables 2 and 3 show the standard protocol for treatment of nerve agent casualties which includes administration of atropine as the gold standard antidote for nerve agent therapy and oxime as a complementary treatment which has a significant role in treatment of patients with nerve agent intoxication, as well as diazepam. Tables 2 and 3 show the standard protocol for treatment of nerve agent casualties which includes administration of atropine as the gold standard antidote for nerve agent therapy and oxime as a complementary treatment which has a significant role in treatment of patients with nerve agent intoxication, as well as diazepam.
No antidote for nerve agent poisoning, or pre-treatment when an attack is likely, is without danger, but faced with a choice between nerve agent poisoning and the side-effects of an antidote, the choice is clear. Untreated recovery can take months before the AChE levels are back to normal. [Pg.219]

The atropine works quickly to block the receptor site for the nerve transmitter acetylcholine. This helps prevent the constant firing of the nerves and gives relief of the symptoms. The 2-PAM is a true antidote and it breaks the bond that has formed between the nerve agent and the enzyme acetylcholinesterase. This allows the enzyme to break down the acetylcholine. Some kits also include a CANA (con-vulsants antidote for nerve agent) injector for treatment of seizures. CANA injectors... [Pg.41]

HI-6 is considered to be a very promising bispyridin-ium oxime in medical treatment after exposure to most nerve agents. For these reasons, HI-6 is involved in the equipment of the Czech, Slovak, Swedish, and Canadian Armies as an antidote against nerve agent intoxication (Bajgar, 2010 Masson, 2011) and is under development in other countries (Lundy et al., 2011 Masson, 2011 Jokanovid, 2012). A disadvantage of HI-6 compared with... [Pg.1063]

Fusek, J. and J. Bajgar. "Antidotal Treatment of Intoxication with New Nerve Agent G V." In Proceedings of the CB Medical Treatment Symposium an Exploration of Present Capabilities and Future Requirements for Chemical and Biological Medical Treatment. Edgewood, MD Battelle Memorial Institute, 1994, 6.6—6.8. [Pg.102]

Dr. Aghajanian also tried the nerve agent GB (sarin) as a possible antidote. It worked quite well, as did VX, another well-known lethal nerve agent. He and Dr. Sidell sueeessfully used both drugs to reverse EA 3580 intoxieation. If not for the general publie fear of anything to do with nerve gas, one might reeommend sarin or VX as superior antidotes to use in the treatment of dmg-indueed delirium. [Pg.115]

The pX a (6.5-8.2) and nucleophilicity of MINA, 44, and of a series of aliphatic oximes derived from it, were found to be consistent with their ability to reactivate AChE inhibited by the nerve agents, sarin and VX. Yet, despite their ability to significantly reactivate AChE in the brains of sarin-intoxicated rats, these aliphatic oximes are not used as antidotes for treatment of OP poisoning in humans this is presumably due to their poor stability in aqueous solution and to their rapid clearance from the circulation. [Pg.642]

General supportive care should be provided as outlined above. Extra precautions should be taken to ensure that rescuers and health care providers are not poisoned by exposure to contaminated clothing or skin. This is especially critical for the most potent substances such as parathion or nerve gas agents. Antidotal treatment consists of atropine and pralidoxime (see Table 58-4). Atropine is an effective competitive inhibitor at muscarinic sites but has no effect at nicotinic sites. Pralidoxime given early enough is capable of restoring the cholinesterase activity and is active at both muscarinic and nicotinic sites. [Pg.1259]

The choice of appropriate treatment for nerve agent intoxication depends on the agent as well as extent and route(s) of exposure. Very mild exposure to nerve agent vapor may necessitate only decontamination and observation severe exposure to vapor or liquid requires immediate decontamination, antidote administration, artificial respiration, monitoring, and supportive therapy over hours to multiple days (ATSDR, 2007 Sidell, 1997 Vale et al, 2007 Pulley and Jones, 2008). Convenient triage classifications have been developed by ATSDR (2007) in collaboration with the US Army Medical Research Institute of Chemical Defense. [Pg.58]

Among promising candidates as antidotes against CNS intoxication by OP nerve agents, memantine (MEM) has been shown to pose both anti-excitotoxic and anti-epileptic properties. Memantine is an uncompetitive NMDA receptor antagonist, clinically used for the treatment of Alzheimer s disease, Parkinson s disease and spasticity, in the absence of serious side effects (Ozsuer et al, 2005 Lipton, 2005). From a series of rat in vivo experiments, it is evident that pre-administration of memantine significantly protects... [Pg.644]

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]


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