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Battlefield Chemical Inhalation Injury
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
The respiratory control center (guinea pig studies) shows spontaneous return of function approximately 1 hr after poisoning. Loss of function at this center does not disappear with repeat dosing with Soman, suggesting that this depressant effect is not AChE-mediated. Soman is particularly rapidly toxic when exposure is by the percutaneous route, with the rate of onset of toxicity approaching that of the inhalational route. Ocular exposures are rapidly toxic as well (Adams et al., (1972).
Insecticides
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
The OP insecticides were originally developed as nerve gases for use as possible chemical warfare agents during World War II. The first of these compounds was TEPP. The biological action of the nerve gases, such as sarin, tabun, and soman, is similar to, but more toxic than, that of the OPs. Soman is not only the most toxic of the three but one of the most toxic compounds ever synthesized, with fatalities occurring with an oral dose of 10 μg/kg in humans (see Chapter 34).
Chemistries of Chemical Warfare Agents
Published in Brian J. Lukey, James A. Romano, Salem Harry, Chemical Warfare Agents, 2019
Terry J. Henderson, Ilona Petrikovics, Petr Kikilo, Andrew L. Ternay Jr., Harry Salem
General Remarks: The discovery of soman in the summer of 1944 by the Austrian-German biochemist Richard Kuhn was the result of a systematic search for compounds that directly inhibit AChE. As was the case for tabun and sarin, soman was initially developed for use as an insecticide, but it proved to be substantially more toxic than the other two OPs. The results were quickly shared with the German Army Weapons Office, as were samples of soman, which led to the production of the compound for use as a CWA. Thickened soman (TGD, also known as VR-55) is created by adding a thickening agent to soman.
Anticonvulsant effectiveness of scopolamine against soman-induced seizures in African green monkeys
Published in Drug and Chemical Toxicology, 2022
John H. McDonough, Joseph D. McMonagle, Benedict R. Capacio
The dose of soman produced a predictable and rapid progression of severe signs of nerve agent intoxication in all animals. Within a minute or so of soman injection, the animals developed chewing and/or facial automatisms. This was immediately followed by mild and intermittent tremor in the limbs, which shortly progressed to strong and continuous tremor in the whole body accompanied by facial grimacing. This phase was soon followed by uncoordinated thrashing movements that rapidly progressed to whole-body convulsions, EEG seizures, loss of posture, and unresponsiveness to external stimuli. Electrographic seizure onset occurred rapidly after soman administration (mean = 4.3 min; 3.3–5.3 min = 95% confidence limits: N = 10). During the seizures and intraictal periods the animals were totally unresponsive to handling and had no eye blink response.
Effect of cholinergic crisis on the potency of different emergency anaesthesia protocols in soman-poisoned rats
Published in Clinical Toxicology, 2019
Katharina Marquart, Julia Herbert, Niko Amend, Horst Thiermann, Franz Worek, Timo Wille
The animals were placed on a heated operating table in supine position and the cannulation of the carotid artery for blood pressure (BP) measurement was performed. After tracheotomy, the cannula was fixed with sutures and ventilation (room air, 80 breaths per min, 6 ml/kg, max. 15 cmH2O peak inspiratory pressure (PIP); VentElite, Harvard Apparatus) and BP measurement (HSE PLUGSYS® TAM-A, Hugo Sachs Electronics, March-Hugstetten, Germany) were started. Also, electrocardiogram (ECG) (HSE PLUGSYS® ECGA, Hugo Sachs Electronics) leads and a rectal thermal probe (HSE PLUGSYS® TCAM, Hugo Sachs Electronics) were inserted. After an adaptation phase for at least 20 min, animals of the soman groups were challenged with ∼2.5 × LD50 soman s.c. (200 µg/kg) and in both soman-atropine groups, 10 mg/kg atropine was injected i.m. 1 min later [29–33]. The reflexes, HR, BP and internal body temperature (IBT) were monitored every 5 min until the end of the experiment (90 min) or death of the animal. Additionally, clinical signs of soman-poisoning were recorded. Blood samples (100 µl) were drawn at time points −1, +5, +15, +30, +45, +60, +90 min for AChE activity analysis. The blood volume was substituted with twice the amount of Ringer’s solution. At the end of the experiments, the animals were euthanized by decapitation.
Novichok: a murderous nerve agent attack in the UK
Published in Clinical Toxicology, 2018
J. Allister Vale, Timothy C. Marrs, Robert L. Maynard
Sidell [15] has reviewed the features and treatment in two patients poisoned with sarin and soman, respectively, and Sidell [16] has reviewed the features of nerve agent poisoning, which can follow inhalation, ingestion or dermal exposure, although the onset of systemic toxicity is slower with the latter. Miosis, which can be painful and last several days, occurs rapidly after ocular exposure to a nerve agent and appears to be a very sensitive index of exposure [17]. Ciliary muscle spasm can impair accommodation, and conjunctival injection and eye pain can occur. Contact with liquid nerve agent can produce localized sweating and fasciculation, which can spread to involve whole muscle groups. Chest tightness, increased salivation, rhinorrhea and bronchorrhea occur within seconds or minutes of inhaling a nerve agent. In contrast, ingestion of food or water contaminated with a nerve agent can cause abdominal pain, nausea, vomiting, diarrhea and involuntary defecation, although the onset of symptoms may be delayed. Miosis can also occur as a systemic feature, although it more usually follows direct exposure. Abdominal pain, nausea and vomiting, involuntary micturition and defaecation, muscle weakness and fasciculation, tremor, restlessness, ataxia and convulsions can follow dermal exposure, inhalation or ingestion of a nerve agent. If exposure is substantial, death may occur from respiratory failure within minutes, whereas mild or moderately exposed individuals usually recover completely, although electroencephalogram abnormalities have been reported in those severely exposed to sarin in Japan [18,19].