ArticleBasic research in cardiology2013
Endothelial NOS (NOS3) impairs myocardial function in developing sepsis.
Article in Basic research in cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- Natural products as multi‑target therapies for sepsis‑induced myocardial dysfunction (Review).International journal of molecular medicine · 2026Review
- Nitric oxide in sepsis: pathophysiological mechanisms and therapeutic implications.Open life sciences · 2026Article
- Norepinephrine exacerbates LPS-induced cardiomyopathy via SIRT3/HO-1 axis-mediated ferroptosis.Critical care (London, England) · 2025Article
- LASSO regression shows histidine and sphingosine 1 phosphate are linked to both sepsis mortality and endothelial damage.European journal of medical research · 2024Article
- Sepsis‑induced cardiac dysfunction and pathogenetic mechanisms (Review).Molecular medicine reports · 2023Review
- Lipid oxidation dysregulation: an emerging player in the pathophysiology of sepsis.Frontiers in immunology · 2023Review
- Research Progress on the Mechanism and Management of Septic Cardiomyopathy: A Comprehensive Review.Emergency medicine international · 2023Review
- The Effect of Sepsis on Myocardial Function: A Review of Pathophysiology, Diagnostic Criteria, and Treatment.Cureus · 2022Review
- Article
- Acute Heart Failure After Reperfused Ischemic Stroke: Association With Systemic and Cardiac Inflammatory Responses.Frontiers in physiology · 2021Article
- An update on the CHDGKB for the systematic understanding of risk factors associated with non-syndromic congenital heart disease.Computational and structural biotechnology journal · 2021Article
- Nitric oxide in cellular adaptation and disease.Redox biology · 2020Review
- Anaemia is associated with severe RBC dysfunction and a reduced circulating NO pool: vascular and cardiac eNOS are crucial for the adaptation to anaemia.Basic research in cardiology · 2020Article
- Mitochondrial bioenergetics links inflammation and cardiac contractility in endotoxemia.Basic research in cardiology · 2019Article
- Whole body periodic acceleration improves survival and microvascular leak in a murine endotoxin model.PloS one · 2019Article
- The Effect of Chemerin on Cardiac Parameters and Gene Expressions in Isolated Perfused Rat HeartBalkan medical journal · 2019Article
- Cardiovascular disease and resuscitated septic shock lead to the downregulation of the HIntensive care medicine experimental · 2017Article
- Septic cardiomyopathy: evidence for a reduced force-generating capacity of human atrial myocardium in acute infective endocarditis.Innovative surgical sciences · 2017Article
- Sepsis-Induced Cardiomyopathy: Oxidative Implications in the Initiation and Resolution of the Damage.Oxidative medicine and cellular longevity · 2017Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial nitric oxide synthase (NOS)3-derived nitric oxide (NO) modulates inotropic response and diastolic interval for optimal cardiac performance under non-inflammatory conditions. In sepsis, excessive NO production plays a key role in severe hypotension and myocardial dysfunction. We aimed to determine the role of NOS3 on myocardial performance, NO production, and time course of sepsis development. NOS3(-/-) and C57BL/6 wildtype mice were rendered septic by cecum ligation and puncture (CLP). Cardiac function was analyzed by serial echocardiography, in vivo pressure and isolated heart measurements. Cardiac output (CO) increased to 160 % of baseline at 10 h after sepsis induction followed by a decline to 63 % of baseline after 18 h in wildtype mice. CO was unaltered in septic NOS3(-/-) mice. Despite the hyperdynamic state, cardiac function and mean arterial pressure were impaired in septic wildtype as early as 6 h post CLP. At 12 h, cardiac function in septic wildtype was refractory to catecholamines in vivo and respective isolated hearts showed impaired pressure development and limited coronary flow reserve. Hemodynamics remained stable in NOS3(-/-) mice leading to significant survival benefit. Unselective NOS inhibition in septic NOS3(-/-) mice diminished this survival benefit. Plasma NO( x )- and local myocardial NO( x )- and NO levels (via NO spin trapping) demonstrated enhanced NO( x )- and bioactive NO levels in septic wildtype as compared to NOS3(-/-) mice. Significant contribution by inducible NOS (NOS2) during this early phase of sepsis was excluded. Our data suggest that NOS3 relevantly contributes to bioactive NO pool in developing sepsis resulting in impaired cardiac contractility.
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Registered trials
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