{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T13:54:05Z","timestamp":1791035645558,"version":"4.1.0"},"reference-count":20,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[2003,5,1]],"date-time":"2003-05-01T00:00:00Z","timestamp":1051747200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hum Exp Toxicol"],"published-print":{"date-parts":[[2003,5]]},"abstract":"<jats:p>\n                    Nerve 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 \u2018skin model\u2019 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 LD\n                    <jats:sub>50<\/jats:sub>\n                    (120 mg\/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\n                    <jats:sup>\/<\/jats:sup>\n                    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.\n                  <\/jats:p>","DOI":"10.1191\/0960327103ht359oa","type":"journal-article","created":{"date-parts":[[2003,5,15]],"date-time":"2003-05-15T19:36:43Z","timestamp":1053027403000},"page":"255-261","source":"Crossref","is-referenced-by-count":49,"title":["Clinical manifestations of VX poisoning following percutaneous exposure in                 the domestic white pig"],"prefix":"10.1177","volume":"22","author":[{"given":"R P","family":"Chilcott","sequence":"first","affiliation":[{"name":"Dstl Biomedical Sciences, Porton Down, Salisbury, Wiltshire, SP4 0JQ, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C H","family":"Dalton","sequence":"additional","affiliation":[{"name":"Dstl Biomedical Sciences, Porton Down, Salisbury, Wiltshire, SP4 0JQ, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I","family":"Hill","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C M","family":"Davidson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K L","family":"Blohm","sequence":"additional","affiliation":[{"name":"Kinchyle Enterprises Inc., PO Box 4000, Station Main, Medicine Hat,                         Alberta, Canada T1A 8K6"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M G","family":"Hamilton","sequence":"additional","affiliation":[{"name":"Medical Therapy Group, Defence Research Establishment Suffi eld, PO Box                         4000, Station Main, Medicine Hat, Alberta, Canada T1A 8K6"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2003,5,1]]},"reference":[{"key":"atypb1","first-page":"83","volume-title":"Chemical warfare agents: toxicology and treatment. 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