Sarin 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. 

A special issue from this Japanese experience are ocular effects of poisoning with sarin and their treatment. Some authors unsuccessfully treated strong miosis and consequential visual darkness with systemic atropine [15, 29], Others used 0.25% or 1.0% atropine sulphate eye drops, but these patients complained of atropine-induced photophobia and poor focusing [25], Our suggestion for optimal treatment of ocular manifestations of intoxication with organophosphorus cholinesterase inhibitors is topical use of pralidoxime chloride eye drops instead of atropine [42], Ocular pain should be treated with tropicamide 0.5% [28],... 

The oxime 2-pralidoxime chloride (2-PAMC1) was administered by slow intravenous infusion to subjects who had received sarin. The half-time for in vivo aging of the sarin-erythrocyte complex seemed to be about 5 h (Sided and Groff, 1974). 

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. 

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... 

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