Dataset Information

Oxidative stress-induced endothelial dysfunction and decreased vascular nitric oxide in COVID-19 patients.

ABSTRACT:

Background

SARS-CoV-2 targets endothelial cells through the angiotensin-converting enzyme 2 receptor. The resulting endothelial injury induces widespread thrombosis and microangiopathy. Nevertheless, early specific markers of endothelial dysfunction and vascular redox status in COVID-19 patients are currently missing.

Methods

Observational study including ICU and non-ICU adult COVID-19 patients admitted in hospital for acute respiratory failure, compared with control subjects matched for cardiovascular risk factors similar to ICU COVID-19 patients, and ICU septic shock patients unrelated to COVID-19.

Findings

Early SARS-CoV-2 infection was associated with an imbalance between an exacerbated oxidative stress (plasma peroxides levels in ICU patients vs. controls: 1456.0 ± 400.2 vs 436 ± 272.1 mmol/L; P < 0.05) and a reduced nitric oxide bioavailability proportional to disease severity (5-α-nitrosyl-hemoglobin, HbNO in ICU patients vs. controls: 116.1 ± 62.1 vs. 163.3 ± 46.7 nmol/L; P < 0.05). HbNO levels correlated with oxygenation parameters (PaO₂/FiO₂ ratio) in COVID-19 patients (R² = 0.13; P < 0.05). Plasma levels of angiotensin II, aldosterone, renin or serum level of TREM-1 ruled out any hyper-activation of the renin-angiotensin-aldosterone system or leucocyte respiratory burst in ICU COVID-19 patients, contrary to septic patients.

Interpretation

Endothelial oxidative stress with ensuing decreased NO bioavailability appears as a likely pathogenic factor of endothelial dysfunction in ICU COVID-19 patients. A correlation between NO bioavailability and oxygenation parameters is observed in hospitalized COVID-19 patients. These results highlight an urgent need for oriented research leading to a better understanding of the specific endothelial oxidative stress that occurs during SARS-CoV-2.

Funding

Stated in the acknowledgments section.

SUBMITTER: Montiel V

PROVIDER: S-EPMC8865837 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature

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Publications

Oxidative stress-induced endothelial dysfunction and decreased vascular nitric oxide in COVID-19 patients.

Montiel Virginie V Lobysheva Irina I Gérard Ludovic L Vermeersch Marjorie M Perez-Morga David D Castelein Thomas T Mesland Jean-Baptiste JB Hantson Philippe P Collienne Christine C Gruson Damien D van Dievoet Marie-Astrid MA Persu Alexandre A Beauloye Christophe C Dechamps Mélanie M Belkhir Leïla L Robert Annie A Derive Marc M Laterre Pierre-François PF Danser A H J AHJ Wittebole Xavier X Balligand Jean-Luc JL

EBioMedicine 20220223

<h4>Background</h4>SARS-CoV-2 targets endothelial cells through the angiotensin-converting enzyme 2 receptor. The resulting endothelial injury induces widespread thrombosis and microangiopathy. Nevertheless, early specific markers of endothelial dysfunction and vascular redox status in COVID-19 patients are currently missing.<h4>Methods</h4>Observational study including ICU and non-ICU adult COVID-19 patients admitted in hospital for acute respiratory failure, compared with control subjects matc ...[more]

PMID: 35219085

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Dataset Information

Oxidative stress-induced endothelial dysfunction and decreased vascular nitric oxide in COVID-19 patients.

Background

Methods

Findings

Interpretation

Funding

Publications

Oxidative stress-induced endothelial dysfunction and decreased vascular nitric oxide in COVID-19 patients.

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