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Soman pralidoxime chloride

Nerve Agent Antidote Kit (NAAK or MARK I) consists of an atropine auto-injector (2 mg), a pralidoxime chloride auto-injector (2-Pam-Cl, 600 mg), the plastic clip joining the two injectors, and a foam case. The kit serve as a countermeasure to nerve agents, including tabun (GA), sarin (GB), soman (GD), GF, and VX. Military personnel can receive three MARK I for self/buddy aid. Possible side effects of atropine and/or 2-PAM-C1 are deemed insignificant in a nerve agent casualty. Intravenous atropine and 2-PAM-C1 can also be made available. The MARK I kit is manufactured by Survival Technology, Inc., Rockville, Maryland. [Pg.67]

If rhinorrhea or bronchorrhea develops, atropine 2 mg in an adult (20 qg kg 1 in a child) should be administered intravenously every 5-10 min until secretions are minimal and the patient is atropinized (dry skin and sinus tachycardia). In all patients receiving atropine, an oxime, such as pralidoxime chloride or mesilate, should be administered in a dose of 30 mg kg-1 body weight intravenously, followed by an infusion of pralidoxime 8-10 mg kg 1 h 1, the infusion rate depending on severity. Alternatively, pralidoxime chloride or mesilate 30 mg kg 1 body weight intravenously can be given every 4-6 h to patients with systemic features. In the case of GF and soman poisoning, consideration should be given to the use of HI-6, if supplies are available. [Pg.258]

There are only a few reports in the open literature on the effect of oximes in nerve agent-exposed humans. Pralidoxime chloride was very effective in reactivating erythrocyte AChE in individuals exposed to sublethal intravenous or oral VX while this oxime was substantially less effective in humans exposed to IV sarin (Sidell and Groff, 1974). Accidental sarin exposure by inhalation resulted in an initial progressive deterioration (coma, apnea) of the patient despite atropine and 2-PAM treatmentand substantial recovery of erythrocyte AChE activity (Sidell, 1974). It took several hours until the patient s condition improved. Sidell also reported an accidental oral soman exposure. A lethal dose of diluted soman splashed into and around the mouth of an individual, resulting in coma, bronchoconstriction and respiratory depression, which was successfully treated with repeated atropine injections. 2-PAM (2 g IV) had no effect on inhibited erythrocyte AChE. [Pg.312]

Carter, W.H., Jones, D.E., and Carchman, R.A. Application of response surface methods for evaluating the interactions of soman, atropine, and pralidoxime chloride. Fundamental and Applied Toxicology 1985 5 S232-S241. [Pg.367]

Pralidoxime was synthesized in the USA in 1955 (Wilson and Ginsburg, 1955). Its four salts - chloride (2-PAM Cl), methiodide, methylsulfate, and mesylate (P2S) - were investigated and introduced into practice. 2-PAM is very efficient in reactivating of AChE inhibited with sarin or VX (Johnson and Stewart, 1970 Sidell and Groff, 1974 Harris and Stitcher, 1983 Mesic et al, 1991 Masuda et al, 1995 Nozaki and Aikawa, 1995), but was not successful in reactivation of the tabun- or soman-inhibited enzyme (Inns... [Pg.990]

Shih, T. etal. (1991) A comparison of cholinergic effects of Hl-6 and pralidoxime-2-chloride (2-PAM) in soman poisoning. Toxicol. Lett., 55.131-147. [Pg.76]


See other pages where Soman pralidoxime chloride is mentioned: [Pg.270]    [Pg.276]    [Pg.294]    [Pg.113]    [Pg.334]    [Pg.335]    [Pg.336]    [Pg.336]    [Pg.230]    [Pg.549]    [Pg.549]    [Pg.207]    [Pg.826]    [Pg.213]    [Pg.592]   
See also in sourсe #XX -- [ Pg.272 ]




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