Experimental estimation of efficiency of antihypoxants at toxic pulmonary edema caused by nitrogen oxide (IV)

Sherbasov, Konstantin A; Basharin, V. A.; Marysheva, V. V.; Kon’shakov, Yury O.; Shabanov, Petr D.

doi:10.17816/rcf14265-68

Cited by 3 publications

(1 citation statement)

References 2 publications

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“…Увеличение же гематокрита (т.е. объема клеток крови) у животных, получивших лечение комбинацией препаратов, вероятно, связано с механизмом ее лечебного действия, а именно активацией газообменной функции крови как следствие компенсаторной реакции системы крови на гипоксию [9].…”

Section: результаты и их обсуждениеunclassified

Experimental therapy for toxic pulmonary edema caused by inhalation poisoning with nitrogen oxides

Torkunov

Zemlyanoi²,

Varlashova³

et al. 2023

Psychopharmacology & biological narcology

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BACKGROUND: Morphological studies conducted in different phases of toxic pulmonary edema initiated by nitrogen oxides have revealed changes in blood vessels and blood cells that develop at the earliest stages of the lesion and precede edema. AIM: To examine the cellular composition of the blood of mice in the presence of inhalation poisoning with nitrogen oxides. MATERIALS AND METHODS: The toxic lung edema was modeled in mice by inhalation of toxic doses of nitrogen oxides LСt50. Blood cells were determined using a hematological analyzer 0.5, 3, and 24 h after poisoning. Parts of the animals, 30 min after the poisoning, were injected intraperitoneally with a complex of drugs consisting of sodium dimercaptopropane sulfonate (unithiol) 150 mg/kg, diclofenac sodium 35.0 mg/kg, and аprotinin (contrikal) 250 IU / kg. RESULTS: In mice poisoned with nitrogen oxides, the main differences were observed in the leukocyte count, composition of the leukocyte formula, and platelet count. Thrombocytosis is observed 3 and 24 h after intoxication. The earliest manifestation of blood poisoning (0.5 h) was a decrease in the total leukocyte count (leukopenia). During the pronounced clinical manifestations of nitric oxide poisoning (3 h), a change in the leukocyte formula toward an increase in the proportion of granulocytes and medium cells (granulocytosis and eosinophilia-monocytosis) was noted. A day after the poisoning, the noted indicators generally return to the initial level. Treatment of poisoned animals with a combination of drugs neutralizes the observed effects. CONCLUSION: The combination of drugs consisting of sodium dimercaptopropane sulfonate (unithiol), diclofenac sodium, and аprotinin (contrikal) was found to be effective in the treatment of toxic lung edema induced by nitrogen oxides.

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Section: результаты и их обсуждениеunclassified

Experimental therapy for toxic pulmonary edema caused by inhalation poisoning with nitrogen oxides

Torkunov

Zemlyanoi²,

Varlashova³

et al. 2023

Psychopharmacology & biological narcology

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Acute chemical pulmonary edema with inhaled nitrogen dioxide intoxication

Tolkach,

Kuznetcov,

Basharin

et al. 2023

Bulletin of the Russian Military Medical Academy

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Nitrogen dioxide is released by the interaction of some metals with nitric acid. Inhalation intoxication with nitrogen dioxide leads to chemical pulmonary edema. This study presents the case of a patient who had acute inhalation exposure to an unidentified brown gaseous substance (presumably nitrogen dioxide) when he etched a metal product with nitric acid. Twenty-four hours after contact with the gas, he manifested signs of intoxication, such as chest pain, tachypnea, and decreased saturation. Laboratory tests revealed hemoconcentration, hyperfermentemia, and arterial hypoxemia. The X-ray image of the entire lung surface revealed a sharp increase and deformation of the pulmonary pattern due to the vascular component. The diagnosis was T65, i.e., toxic effect of other and unspecified substances. With treatment, the patients condition improved. On day 4 after therapeutic exposure, with decreased oxygen fraction in the inhaled gas mixture to 0.3, the saturation increased to 98%, and tachypnea disappeared. On day 6, with ongoing treatment (oxygen therapy, use of antioxidants, antihypoxants, anti-inflammatory, and antibacterial drugs), the inflammatory reaction stopped, the rheological properties of the blood improved, and the gas composition of arterial blood normalized, i.e., the oxygenation index was 436, which indicated the disappearance of arterial blood oxygenation disorders. During the radiological examination, the normal radiological picture of the lungs was determined. Thus, on day 6 after the start of therapy, signs of intoxication were completely stopped. Specific changes in the lungs during radiation research techniques, hemoconcentration, inflammation, and hypoxemia during laboratory blood tests should be considered prognostic signs of chemical pulmonary edema. As a pathogenetic therapy, treatment must be supplemented with drugs that stop the cascade of free radical oxidation reactions (acetylcysteine and sodium thiosulfate). Individuals exposed to nitrogen dioxide should be considered a high-risk group for lung damage and hospitalized for dynamic observation for at least 2 days. Taking into account the genotoxic effects of nitrogen dioxide, affected patients should be classified as at risk of developing neoplasms and undergo further dynamic monitoring.

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Therapeutic efficacy of N-cholinolitic drug N,N-Diethyl-5,5-diphenyl-2-pentynylamine in models of non-cardiogenic pulmonary edema

Melikhova

Krasnov

Rozhko

et al. 2023

MES

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The existing non-cardiogenic pulmonary edema (NCPE) treatment methods are not sufficiently effective. N,N-Diethyl-5,5-diphenyl-2-pentynylamine hydrochloride (DDPA), the N-cholinolitic drug, is of interest as a potential remedy for treatment of toxic pulmonary edema (TPE). The study was aimed to determine therapeutic efficacy of the drug in animal TPE models. TPE in white rats was induced through intraperitoneal thiourea injection or nitrogen dioxide inhalation. Treatment of animals involved inhalation of the DDPA aqueous solution. The efficacy was estimated based on the animals’ survival rate and lung gravimetry data. The results were assessed based on descriptive statistics using the Student's t-test. In the model of thiourea-induced NCPE, the drug administered after the toxic exposure increased the animals’ survival rate and significantly decreased lung hydration levels (149% vs. 262.5% in non-treated animals). In the model of nitrogen dioxideinduced NCPE, the drug significantly increased the rats’ survival rate within the period between 0 and 5 h, however, the differences became non-significant within 24 h. The treated animals had 15–20% lower respiratory rate and pulmonary coefficients than non-treated animals 5 h after the NO2 exposure. The use of DDPA improved the survival rate and overall health in both TPE models, however, the thiourea-based model showed better treatment outcomes compared to the NO2–based model. Such differences can be explained by the deeper and more disruptive nature of the lung tissue injury caused by nitrogen dioxide compared to that caused by thiourea. Thus, the use of DDPA in individuals with injuries induced by pulmonotoxic chemicals may be promising at the prehospital stage.

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Experimental estimation of efficiency of antihypoxants at toxic pulmonary edema caused by nitrogen oxide (IV)

Cited by 3 publications

References 2 publications

Experimental therapy for toxic pulmonary edema caused by inhalation poisoning with nitrogen oxides

Experimental therapy for toxic pulmonary edema caused by inhalation poisoning with nitrogen oxides

Acute chemical pulmonary edema with inhaled nitrogen dioxide intoxication

Therapeutic efficacy of N-cholinolitic drug N,N-Diethyl-5,5-diphenyl-2-pentynylamine in models of non-cardiogenic pulmonary edema

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