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 УЧРЕДИТЕЛИ:
Институт теоретической и экспериментальной биофизики Российской академии наук.

ООО "ИЦ КОМКОН"

ФГБУН "Институт токсикологии" ФМБА России




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192012, Санкт-Петербург, ул.Бабушкина, д.82 к.2, литера А, кв.378

Свидетельство о регистрации электронного периодического издания ЭЛ № ФС 77-37726 от 13.10.2009
Выдано - Роскомнадзор

ISSN 1999-6314

Российская поисковая система
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«
Vol. 25, Art. 13 (pp. 205-219)    |    2024       
»

Experimental evaluation of the effectiveness of oxygen and prednisolone for the correction of toxic pulmonary edema caused by intoxication by thermal-destruction products of nitrocellulose
Shapovalov I.D., Yaroshenko D.M., Lopatko V.S., Tolkach P.G., Yazenok A.V.

S.M. Kirov Military Medical Academy, St. Petersburg, Russian Federation



Brief summary

. Relevance. Modern approaches to the treatment of powder gas poisoning are aimed at correcting hemic and respiratory hypoxia; oxygen and glucocorticoids are used for these purposes. To simulate the pathological processes that occur in the body when exposed to powder gases, an experimental model of intoxication with products of thermal destruction of nitrocellulose can be used. Target. In an experiment, to evaluate the effectiveness of the use of oxygen and prednisolone in laboratory animals for the correction of toxic pulmonary edema during intoxication with thermal destruction products of nitrocellulose. Materials and methods. Intoxication of mice with products of thermal destruction of nitrocellulose (1.5HLC50) was modeled. Immediately after exposure, a single normobaric oxygenation (FiO2-0.3 and 0.9) was performed for 30 min. Immediately after exposure, mice were administered prednisolone at a dose of 5 and 160 mg/kg as a single dose. Survival, the average lifespan of mice, lung coefficient 3 and 6 h after exposure, and histological changes in lung tissues obtained 6 h after exposure were assessed. Results. Intoxication of mice with thermal degradation products of nitrocellulose (1.5HLC50) led to the formation of toxic pulmonary edema 6 hours after exposure. Survival of mice treated with oxygen (FiO2-0.3, 25?13% and FiO2-0.9, 17?11%) was lower (p>0.05) compared to untreated animals (33?15%). We found a decrease (p<0.05) in the average lifespan (3.6 [3.1; 4.4] hours) in mice treated with oxygen (FiO2-0.9) compared to animals that did not receive treatment (7.5 [6.7; 8.4] h). At 6 h post-exposure, the pulmonary quotient of oxygen-treated mice (FiO2-0.9) was higher (p<0.05; 32.6 [30.7; 34.8]) compared to untreated animals (23.2 [21.6; 24.4]). The use of prednisolone in the studied regimens did not lead to an increase in survival, average life expectancy and a decrease in pulmonary coefficient compared to animals that did not receive treatment. Conclusion. The use of prednisolone (5 and 160 mg/kg once immediately after exposure) does not contribute to the correction of toxic pulmonary edema caused by intoxication with thermal destruction products of nitrocellulose (1.5 HLC50). The use of oxygen (single normobaric oxygenation (FiO2-0.9), immediately after exposure for 30 min) aggravates the course of toxic pulmonary edema. The use of oxygen in high concentrations immediately after poisoning with powder gases should be justified and performed only if there are clear signs of hypoxia.


Key words

prednisolone, oxygen, treatment, powder gases, thermal destruction products of nitrocellulose, toxic pulmonary edema.





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