Experimental study of the comparative effectiveness of the use of oxygen, zinc bisvinylimidazole diacetate, and ascorbic acid for the correction of intoxication by thermal destruction products of nitrocellulose

The effectiveness of the use of oxygen, zinc bisvinylimidazole diacetate, and ascorbic acid for the treatment of powder gas poisoning was evaluated using an intoxication model of laboratory animals (mice) with thermal destruction products of nitrocellulose. Mice were subjected to intoxication with thermal destruction products of nitrocellulose in an average lethal concentration. Oxygen therapy (proportion of inhaled oxygen: 0.3; 1 ata) was performed immediately after exposure and once for 30 min. Zinc bisvinylimidazole diacetate (9 mg/kg, intraperitoneal) and ascorbic acid (40 mg/kg, intraperitoneal) were administered to mice once after exposure. Survival rate, hemoglobin derivative concentrations, pulmonary coefficient, and histological changes in the lung tissue were determined. The effectiveness of the use (protection, antidote power, and guaranteed protection indices) of a combination of zinc bisvinylimidazole diacetate and ascorbic acid was assessed. The survival rate of mice that received oxygen after intoxication with thermal destruction products of nitrocellulose was lower (20 ± 13%; p < 0.05) than that of animals that did not receive treatment (60 ± 16%); 3 h after exposure, the pulmonary coefficient was 22.5 [21.9; 23.8] rel. units and 13.1 [12.5; 13.7] rel. units respectively. The protection index of the combination of zinc bisvinylimidazole diacetate and ascorbic acid was 1.39 rel. units, antidote power indicator was 0.95 rel. units, and guaranteed protection coefficient was 0.65 rel. units. The use of the study combination resulted in decreased carboxyhemoglobin (9.3 [7.8, 12.9]%; p < 0.05) and methemoglobin (2.4 [1.5, 4.1]%; p < 0.05) concentrations compared to animals that did not receive treatment (24.5 [22.9; 28.3]% and 8.9 [7.3; 11.1]%, respectively). The pulmonary coefficient of mice receiving the study drug combination was lower (p < 0.05) than that of animals not receiving treatment at 3 and 6 h after exposure. Moreover, 6 h after exposure, signs of the alveolar phase were determined in mice that did not receive treatment, and in animals that were administered the study drug combination, signs of the interstitial phase of toxic pulmonary edema were observed. Thus, the use of oxygen after intoxication with products of thermal destruction of nitrocellulose leads to early formation of toxic pulmonary edema. As a pathogenetically based approach to the treatment of intoxication, the use of zinc bisvinylimidazole diacetate and ascorbic acid should be considered, the mechanism of action of which is aimed at relieving hemic and respiratory hypoxia.