scholarly journals Modelling of Inhalation Poisoning with Sulphur Mustard Gas

Biomeditsina ◽  
2020 ◽  
Vol 16 (3) ◽  
pp. 106-110
Author(s):  
K. A. Bulka ◽  
A. A. Kuzmin ◽  
S. P. Sidorov ◽  
O. V. Chubar ◽  
Yu. Sh. Khalimov

The present work describes the currently existing experimental models of sulphur mustard gas inhalation injury. These models were analysed in terms of their suitability for the development of medical protective equipment. It is proposed to use micro-sprayers, which provide the possibility of transferring mustard gas from a liquid state to an aerosol form while exhibiting an increased ergonomic simplicity and safety.

Biomeditsina ◽  
2020 ◽  
Vol 16 (3) ◽  
pp. 111-114
Author(s):  
K. A. Bulka ◽  
S. P. Sidorov ◽  
O. V. Chubar ◽  
M. A. Metelitsa

The current work assesses the efficacy of a course of intramuscular administration of dexamethasone at doses of 1 or 4 mg/kg when modelling sulphur mustard aerosol inhalation injury. To this end, the average lethal doses, the median death time and the protection coefficients were calculated for rats with sulphur mustard inhalation injury induced by a micro-sprayer. In the treatment regimen used, dexamethasone showed low levels of efficacy, possibly due to its pleiotropic effect on the immune system.


2014 ◽  
Vol 33 (4) ◽  
pp. 271-281 ◽  
Author(s):  
Brian M. Keyser ◽  
Devon K. Andres ◽  
Wesley W. Holmes ◽  
Danielle Paradiso ◽  
Ashley Appell ◽  
...  

Mustard gas (sulfur mustard [SM], bis-[2-chloroethyl] sulfide) is a vesicating chemical warfare agent and a potential chemical terrorism agent. Exposure of SM causes debilitating skin blisters (vesication) and injury to the eyes and the respiratory tract; of these, the respiratory injury, if severe, may even be fatal. Therefore, developing an effective therapeutic strategy to protect against SM-induced respiratory injury is an urgent priority of not only the US military but also the civilian antiterrorism agencies, for example, the Homeland Security. Toward developing a respiratory medical countermeasure for SM, four different classes of therapeutic compounds have been evaluated in the past: anti-inflammatory compounds, antioxidants, protease inhibitors and antiapoptotic compounds. This review examines all of these different options; however, it suggests that preventing cell death by inhibiting apoptosis seems to be a compelling strategy but possibly dependent on adjunct therapies using the other drugs, that is, anti-inflammatory, antioxidant, and protease inhibitor compounds.


1919 ◽  
Vol 157 (6) ◽  
pp. 808-825 ◽  
Author(s):  
George W. Covey ◽  
Moses Baukon
Keyword(s):  

Author(s):  
Saurabh Aggarwal ◽  
Ahmed Lazrak ◽  
Israr Ahmad ◽  
Zhihong Yu ◽  
Ayesha Bryant ◽  
...  

ABSTRACTWe previously reported that cell-free heme (CFH) is increased in the plasma of patients with acute and chronic lung injury and causes pulmonary edema in animal model of acute respiratory distress syndrome (ARDS) post inhalation of halogen gas. However, the mechanisms by which CFH causes pulmonary edema are unclear. Herein we report for the first time the presence of CFH and chlorinated lipids (formed by the interaction of halogen gas, Cl2, with plasmalogens) in the plasma of patients and mice exposed to Cl2 gas. Ex vivo incubation of red blood cells (RBC) with halogenated lipids caused oxidative damage to RBC cytoskeletal protein spectrin, resulting in hemolysis and release of CFH. A single intramuscular injection of the heme-scavenging protein hemopexin (4 µg/kg body weight) in mice, one hour post halogen exposure, reversed RBC fragility and decreased CFH levels to those of air controls. Patch clamp and short circuit current measurements revealed that CFH inhibited the activity of amiloride-sensitive (ENaC) and cation sodium (Na+) channels in mouse alveolar cells and trans-epithelial Na+ transport across human airway cells with EC50 of 125 nM and 500 nM, respectively. Molecular modeling identified 22 putative heme-docking sites on ENaC (energy of binding range: 86-1563 kJ/mol) with at least 2 sites within its narrow transmembrane pore, potentially capable of blocking Na+ transport across the channel. In conclusion, results suggested that CFH mediated inhibition of ENaC activity may be responsible for pulmonary edema post inhalation injury.


CHEST Journal ◽  
1991 ◽  
Vol 100 (5) ◽  
pp. 1436-1441 ◽  
Author(s):  
Lutz Freitag ◽  
Nosrat Firusian ◽  
Georg Stamatis ◽  
Dieter Greschuchna

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Mostafa Ghanei ◽  
Marco Chilosi ◽  
Hassan Mohammad Hosseini Akbari ◽  
Rouzbeh Motiei-Langroudi ◽  
Ali Amini Harandi ◽  
...  

We performed a pathologic study with further using an immunohistochemical technique (using anti-p63 and anti-CK5) on tissues obtained by open lung biopsy from 18 patients with previous exposure to sulphur mustard (SM) as case group and 8 unexposed patients (control group). The most frequent pathologic diagnosis was constrictive bronchiolitis (44.4%), followed by respiratory (22.2%) and chronic cellular bronchiolitis (16.7%) in the case group, and hypersensitivity bronchiolitis (50%) in the control group. The pathologic diagnoses were significantly different in the case and control groups (P=0.042). In slides stained by anti-p63 and anti-CK5, the percent of stained cells and the mean number of epithelial cells were lower in the case group in comparison to the control group. This difference was significant for the mean number of cells stained by anti-CK5 (P=0.042). Furthermore, there was a significant correlation between pathologic diagnosis and total number of cells and mean number of cells stained with anti-p63 and anti-CK5 (P  value = 0.002, <0.001, 0.044). These results suggest that constrictive bronchiolitis may be the major pathologic consequence of exposure to SM. Moreover, decrease of p63 in respiratory tissues affected by SM may suggest the lack of regenerative capacity in these patients.


2020 ◽  
Vol 118 (15) ◽  
pp. e1725671 ◽  
Author(s):  
R. Bhuvaneswari ◽  
J. Princy Maria ◽  
V. Nagarajan ◽  
R. Chandiramouli

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