On the question of studying hyperoxic sanogenesis SARS-CoV-2-associated pneumonia

P. Savilov
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Abstract

The article is devoted to the analysis of literature data on the use of hyperbaric oxygenation (HBO) in patients with COVID-19, complicated by the development of SARS-CoV-2-associated pneumonia to build a hypothesis about possible mechanisms of therapeutic action of hyperbaric oxygen (HBO2) in this pathology. The expediency of using «soft» (1.3–2.0 attacks, 40–60 min) HBO modes in SARS-CoV-2-associated pneumonia is substantiated. Several possible mechanisms of elimination of HBO2 violation of lung gas exchange function in SARS-CoV-2-associated pneumonia are considered. Firstly, hyperoxic stimulation of diaphragm contraction. Secondly, the inhibitory effect of HBO2 on the development of interstitial and alveolar edema in the lungs. Thirdly, elimination of HBO2 stimulating effect of thrombin and fibrinogen on contractility of pulmonary capillary endotheliocytes. Fourth, regulation of HBO2 metabolism of fibronectin, thromboplastin, von Willibrant factors, and platelet activation factor in the wall of pulmonary capillaries. As a result, its thrombogenic activity increases in this pathology.
关于sars - cov -2相关性肺炎的高氧生血研究问题
本文旨在通过对新冠肺炎合并sars - cov -2相关性肺炎患者高压氧(HBO)治疗的文献资料进行分析,提出高压氧(HBO2)治疗新冠肺炎的可能机制假说。证实了在sars - cov -2相关肺炎中使用“软”(1.3-2.0攻击,40-60分钟)HBO模式的便利性。考虑了在sars - cov -2相关性肺炎中消除HBO2破坏肺气体交换功能的几种可能机制。首先,高氧刺激膈肌收缩。其次,HBO2对肺间质水肿和肺泡水肿的抑制作用。第三,消除凝血酶和纤维蛋白原对肺毛细血管内皮细胞收缩力的HBO2刺激作用。第四,肺毛细血管壁中纤连蛋白、凝血活素、血小板活化因子、血小板活化因子的HBO2代谢调控。因此,在这种病理中,其血栓形成活性增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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