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- W3176528963 abstract "Background: Vascular injury has been implicated as a major cause of clinical complications in patients with coronavirus disease 2019 (COVID-19) based on autopsy studies showing destruction of the endothelial architecture. Red blood cells (RBCs) are affected by COVID-19 with alterations in their structure and function, possibly altering disease progress. Objectives: This study was designed to test the hypothesis of persistent endothelial dysfunction and that RBCs act as mediators of endothelial dysfunction in COVID-19. Methods and results: COVID-19 patients displayed profound endothelial dysfunction in vivo assessed with pulse amplitude tonometry, both in the acute phase and at follow-up four months later. RBCs from COVID-19 patients in the acute phase incubated with healthy rat aorta induced severe endothelial dysfunction ex vivo compared to RBCs from healthy subjects. Further, these RBCs induced upregulation of vascular arginase 1 and oxidative stress. Consequently, inhibition of vascular arginase or superoxide attenuated endothelial dysfunction induced by RBCs from COVID-19 patients. These RBCs were characterized by increased production of reactive oxygen species and reduced export of the nitric oxide metabolite nitrate. RBCs from COVID-19 patients at follow-up did not affect endothelial function. Pre-incubation of RBCs from healthy subjects with interferon-γ impaired endothelial function.Conclusions: This study demonstrates the presence of persistent endothelial dysfunction in an otherwise mainly healthy population hospitalized for COVID-19, and clearly implicates a central role of RBCs as mediators of endothelial injury. These data shed light on a new pathological mechanism underlying vascular dysfunction in COVID-19 and may lay the foundation for future therapeutic developments." @default.
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- W3176528963 date "2021-01-01" @default.
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- W3176528963 title "Erythrocytes Induce Vascular Dysfunction in COVID-19" @default.
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- W3176528963 doi "https://doi.org/10.2139/ssrn.3945298" @default.
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