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dc.contributor.authorChilcott, Robert
dc.contributor.authorDalton, C. H.
dc.contributor.authorHill, I.
dc.contributor.authorDavidson, C. M.
dc.contributor.authorBlohm, K. L.
dc.contributor.authorHamilton, M. G.
dc.date.accessioned2013-06-06T07:45:51Z
dc.date.available2013-06-06T07:45:51Z
dc.date.issued2003-05
dc.identifier.citationChilcott , R , Dalton , C H , Hill , I , Davidson , C M , Blohm , K L & Hamilton , M G 2003 , ' Clinical manifestations of VX poisoning following percutaneous exposure in the domestic white pig ' , Human & Experimental Toxicology , vol. 22 , no. 5 , pp. 255-261 . https://doi.org/10.1191/0960327103ht359oa
dc.identifier.issn0960-3271
dc.identifier.otherPURE: 678368
dc.identifier.otherPURE UUID: a040b313-3204-4789-af7a-81d881687e98
dc.identifier.otherWOS: 000182882000005
dc.identifier.otherScopus: 0037799836
dc.identifier.urihttp://hdl.handle.net/2299/10728
dc.description.abstractNerve agents are a class of organophosphorus chemicals that inhibit certain cholinesterase enzymes (ChE). If untreated, percutaneous exposure to nerve agents, such as VX (O-ethyl-S-[2(diisopropylamino)ethyl] methylphosphonothioate) can cause paralysis, apnoea and death. Much of the information concerning the percutaneous absorption and subsequent toxicity of nerve agents has been obtained using various rodent models. However, the most relevant 'skin model' is arguably the pig. Therefore, the purpose of this study was to examine the clinical manifestations of VX intoxication in the domestic white pig following a 2 LD50 (120 mug/kg) percutaneous challenge. There was a consistent onset of signs ( where present) in each animal: mastication was followed by miosis, salivation, fasciculations and apnoea. Whilst ChE activity did not correlate with the onset of signs, there was a qualitative relationship in that mastication preceded substantial ChE inhibition, miosis lagged behind the linear decrease in acetylcholinesterase (AChE) activity and fasciculations and apnoea occurred after maximum ChE inhibition had been attained (5-10% of normal). These observations may be of use for the triage of patients exposed to VX. In comparison with similar studies with GD, VX did not affect glucose utilization. However, VX was similar to GD in that it caused a mild hyperkalaemia and hyperphosphataemia, although the significance of this observation was not clear. There was substantial lateral diffusion of the initial droplet of VX over the application site, indicating that, when decontaminating exposed skin, attention should also be directed to areas peripheral to the original site of exposure.en
dc.format.extent7
dc.language.isoeng
dc.relation.ispartofHuman & Experimental Toxicology
dc.subjectcholinesterase
dc.subjectclinical reference values
dc.subjectnerve agent
dc.subjectpig
dc.subjectskin absorption
dc.subjecttoxicity
dc.subjectMODEL
dc.subjectSWINE
dc.subjectSOMAN
dc.titleClinical manifestations of VX poisoning following percutaneous exposure in the domestic white pigen
dc.contributor.institutionDepartment of Pharmacy
dc.contributor.institutionPharmaceutics
dc.contributor.institutionCentre for Research into Topical Drug Delivery and Toxicology
dc.contributor.institutionToxicology
dc.contributor.institutionSchool of Life and Medical Sciences
dc.contributor.institutionHealth & Human Sciences Research Institute
dc.description.statusPeer reviewed
rioxxterms.versionofrecordhttps://doi.org/10.1191/0960327103ht359oa
rioxxterms.typeJournal Article/Review
herts.preservation.rarelyaccessedtrue


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