S.M. Kirov Military medical academy of the Ministry of Defense of the Russian Federation, 194044, St. Petersburg
Brief summary
In the event of emergencies at chemically hazardous facilities where ammonia is used, it enters the environment with the formation of a focus of chemical damage. Inhalation intake of ammonia leads to the formation of chemical pulmonary edema. To date, approaches to the correction of this pathological condition are very limited. The aim of the study was to develop an experimental model of toxic pulmonary edema during inhalation intoxication of rats with ammonia. Materials and methods. Static inhalation intoxication of rats with chemically obtained ammonia was modeled. The mean lethal concentration (LC50) of ammonia was calculated (exposure 30 min). At various times after exposure, indicators of the vital functions of rats were determined, the gas composition of arterial blood was analyzed, and the value of the pulmonary coefficient was determined. Research results. It was found that the LC50 of ammonia for rats is 35.8?6.4 g/m3 (30 min exposure). During the first 24 hours after exposure, a decrease in respiratory rate, heart rate, SpO2 was determined in laboratory animals compared to control. Severe hypoxemia, hypercapnia and decompensated respiratory acidosis were revealed against the background of an increase in the pulmonary coefficient. Conclusion. As the cause of the lethal outcome of rats, pronounced disorders in the structure and function of the respiratory system of rats due to the manifestation of toxic pulmonary edema caused by ammonia intoxication should be considered. This experimental model can be used to evaluate the effectiveness of the means of correcting acute inhalation ammonia intoxication.
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