Nitric oxide mediated hypoxia dynamics in COVID-19.

Several COVID-19 patients frequently experience with happy hypoxia. Sometimes, the level of nitric oxide (NO) in COVID-19 patients was found to be greater than in non-COVID-19 hypoxemics and most of the cases lower. Induced or inhaled NO has a long history of usage as a therapy for hypoxemia. Excessive production of ROS and oxidative stress lower the NO level and stimulates mitochondrial malfunction is the primary cause of hypoxia-mediated mortality in COVID-19. Higher level of NO in mitochondria also the cause of dysfunction, because, excess NO can also diffuse quickly into mitochondria or through mitochondrial nitric oxide synthase (NOS). A precise dose of NO may increase oxygenation while also acting as an effective inhibitor of cytokine storm. NOS inhibitors may be used in conjunction with iNO therapy to compensate for the patient's optimal NO level. NO play a key role in COVID-19 happy hypoxia and a crucial component in the COVID-19 pathogenesis that demands a reliable and easily accessible biomarker to monitor. • The level of nitric oxide (NO) in COVID-19 patients is much lower than healthy control group which is one of the key factors of hypoxia. • Sometimes, NO was found to be greater in COVID patients than in non-COVID hypoxemics, which is also may be the cause of hypoxia due to mitochondrial failure in excess NO level in cell. • A precise dose of NO may increase oxygenation that might be also effective as the inhibitor of cytokine storm. • NOS inhibitors may be used in conjunction with iNO therapy to compensate for the patient's optimal NO level. [ABSTRACT FROM AUTHOR]