ABSTRACT
Introduction. ARDS (acute respiratory distress syndrome) is a direct cause of death due to lung lesions of various origins including SARS-CoV-2 infection. Most lung and respiratory diseases are characterized by inflammation, which in turn causes occlusions, mucous hypersecretion, shortness of breath, cough and other symptoms of airway inflammation. Understanding the pathological processes involved in the regulation of the immune response may lead to the discovery of new mechanisms that support or suppress inflammatory processes in the lungs and respiratory tract. Methods. In order to develop the experimental model of ARDS we used precision pulmonary hyperventilation and intratracheal administration of poly I:C, which reproduces the body's response to viral infection (mimic viral infection). The severity of ARDS was estimated by the following parameters: the ratio of wet lung weight to dry lung (wet/dry lung weight), extensibility, impedance, lung stiffness, protein level and the number of neutrophils in the bronchial lavage, the level of proinflammatory cytokines in lung tissue. Moreover, we provide a method of simultaneous registration of the lungs vagal nerve activation parameters due to ARDS induction. It is known that the lungs have a massive innervation of the peripheral nervous system and such innervation has a powerful effect on the cells of the immune system. Results. The biologically active substances of neurons affect the activity of immune cells, and the activity of the immune system affects the functioning of the nervous system. That is why the investigation of neuro-immune interaction has a great potential in studying ARDS. Evaluation of dynamic changes in respiratory function due to simulated ARDS showed a significant increase in such parameters as Newtonian resistance, tissue stiffness, static elongation, and a decrease in elasticity and tissue dumping, which is fully consistent with the pathogenesis of ARDS in patients. Analysis of the dry/wet lung ratio showed a two-fold increase in pulmonary edema, a severe, life-threatening condition that develops as a result of ARDS. Significant increase of the protein content and concentration of neutrophils in bronchopulmonary lavage indicates an increase in the permeability of the pulmonary capillaries due to ARDS. The real time PCR identified significant increase of proinflammatory chemokine Cxl2 concentration. Also we observed an increase of neutrophil-activating protein 3 cytokine Gro1, which stimulates the migration of neutrophils. Electrophysiological registration of the activity of the vagal nerve innervating the lungs showed a significant increase in the activity of nociceptive and mechanosensitive fibers, especially in the last stage of acute respiratory distress syndrome, which confirms the role of the nervous system in this pathology. Conclusion. As a result we obtained a model that reproduces ARDS most relevant to human pathological condition.