The novel coronavirus infection COVID-19 is associated with increased release of inflammatory cytokines (cytokine storm) and reactive oxygen species. These processes result a damage to the endothelium, pulmonary alveolar epithelium and their basal membranes (including the structures of blood-air barrier), increased vascular permeability and non-cardiogenic pulmonary edema. These mechanisms underlie the pathogenesis of acute respiratory distress syndrome in patients with coronavirus infection COVID-19. In this review, we have analyzed the data on the effect of lithium chloride on cytokine storm, increased vascular endothelial permeabili-ty, apoptosis of endotheliocyte and advanced activation of innate immune cells in patients with coronavirus infection COVID-19.