ArticleCritical care (London, England)2014
Deeper understanding of mechanisms contributing to sepsis-induced myocardial dysfunction.
Article in Critical care (London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Boerhaave Syndrome-Narrative Review.Diagnostics (Basel, Switzerland) · 2025Review
- Serum S100A12 in the clinical diagnosis of sepsis-induced myocardial dysfunction: an integrated bioinformatics and clinical data analysis.Frontiers in cardiovascular medicine · 2025Article
- Effect of sepsis on the action potential and cardiac serotonin response in rats.Experimental and therapeutic medicine · 2019Article
- P27 Protects Cardiomyocytes from Sepsis via Activation of Autophagy and Inhibition of Apoptosis.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Puerarin attenuates the inflammatory response and apoptosis in LPS-stimulated cardiomyocytes.Experimental and therapeutic medicine · 2016Article
- Haemodynamic Effects of Lung Recruitment Manoeuvres.BioMed research international · 2015Review
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inflammatory response of sepsis results in organ dysfunction, including myocardial dysfunction. Myocardial dysfunction is particularly important in patients with severe septic shock who progress to a hypodynamic pre-terminal phase. Multiple aspects of this septic inflammatory response contribute to the pathogenesis of decreased ventricular contractility. Inflammatory cytokines released by inflammatory cells contribute as does nitric oxide released by vascular endothelium and by cardiomyocytes. Endotoxins and other pathogen molecules induce an intramyocardial inflammatory response by binding Toll-like receptors on cardiomyocytes that then signal via NF-κB. These processes alter cardiomyocyte depolarization and, therefore, contractility. The particular role of the cardiomyocyte sodium current has not been characterized. Now new information suggests that the septic inflammatory response impairs normal depolarization by altering the cardiomyocyte sodium current. This results in decreased ventricular contractility. This is important because new targets for therapeutic intervention can be considered and new approaches to evaluation of this problem can be contemplated.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.