ArticleThe Journal of surgical research2015
Lipopolysaccharide and cytokines inhibit rat cardiomyocyte contractility in vitro.
Article in The Journal of surgical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Role of bacterial pathogens and toxins in sepsis-related myocardial injury: a scoping review.BMJ open · 2026Article
- Natural products as multi‑target therapies for sepsis‑induced myocardial dysfunction (Review).International journal of molecular medicine · 2026Review
- The role of cytokines in septic myocardial dysfunction: a translational systematic review and meta-analysis.Annals of intensive care · 2026Review
- Cfp1 Controls Cardiomyocyte Maturation by Modifying Histone H3K4me3 of Structural, Metabolic, and Contractile Related Genes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Comparison of the Cecum Ligation and Puncture Method and the Intraperitoneal Lipopolysaccharide Injection Method for the Construction of a New-Onset Atrial Fibrillation Model of Sepsis.Journal of inflammation research · 2024Article
- The Apelin/APJ System: A Potential Therapeutic Target for Sepsis.Journal of inflammation research · 2024Review
- Flagellin-Induced Immune Response in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes.International journal of molecular sciences · 2023Article
- Yes-Associated Protein and Transcriptional Coactivator with PDZ-Binding Motif in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- The direct effect of lipopolysaccharide on an isolated heart is different from the effect on cardiac myocytesArchives of medical science : AMS · 2023Article
- YAP/TEAD1 Complex Is a Default Repressor of Cardiac Toll-Like Receptor Genes.International journal of molecular sciences · 2021Article
- Hydrogen Sulfide Attenuated Sepsis-Induced Myocardial Dysfunction Through TLR4 Pathway and Endoplasmic Reticulum Stress.Frontiers in physiology · 2021Article
- The Role of Long Non-coding RNAs in Sepsis-Induced Cardiac Dysfunction.Frontiers in cardiovascular medicine · 2021Review
- Atrial Myocyte NLRP3/CaMKII Nexus Forms a Substrate for Postoperative Atrial Fibrillation.Circulation research · 2020Article
- Minocycline reverses IL-17A/TRAF3IP2-mediated p38 MAPK/NF-κB/iNOS/NO-dependent cardiomyocyte contractile depression and death.Cellular signalling · 2020Article
- Role of complement C5a and histones in septic cardiomyopathy.Molecular immunology · 2018Review
- LncRNACirculation research · 2018Article
- Relationship between CaSRs and LPS-injured cardiomyocytes.International journal of clinical and experimental pathology · 2018Article
- Experimental Sepsis Severity Score Associated to Mortality and Bacterial Spreading is Related to Bacterial Load and Inflammatory Profile of Different Tissues.Inflammation · 2017Article
- Inhibition of NADPH oxidase 2 (NOX2) prevents sepsis-induced cardiomyopathy by improving calcium handling and mitochondrial function.JCI insight · 2017Article
- Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status.Physiological reports · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSepsis-induced cardiomyopathy (SIC) is thought to be the result of detrimental effects of inflammatory mediators on the cardiac muscle. Here we studied the effects of prolonged (24 ± 4 h) exposure of adult rat ventricular myocytes (ARVM) to bacterial lipopolysaccharide (LPS) and inflammatory cytokines tumor necrosis factor (TNF) and interleukins-1 (IL-1) and IL-6. MATERIALS AND
methodsWe measured sarcomere shortening (SS) and cellular calcium (Ca(2+)) transients (ΔCai, with fura-2 AM) in isolated cardiomyocytes externally paced at 5 Hz at 37°C.
resultsSS decreased after incubation with LPS (100 μg/mL), IL-1 (100 ng/mL), and IL-6 (30 ng/mL), but not with lesser doses of these mediators, or TNF (10-100 ng/mL). A combination of LPS (100 μg/mL), TNF, IL-1, and IL-6 (each 100 ng/mL; i.e., "Cytomix-100") induced a maximal decrease in SS and ΔCai. Sarcoplasmic reticulum (SR) Ca(2+) load (CaSR, measured with caffeine) was unchanged by Cytomix-100; however, SR fractional release (ΔCai/CaSR) was decreased. Underlying these effects, Ca(2+) influx into the cell (via L-type Ca(2+) channels, LTCC) and Ca(2+) extrusion via Na(+)/Ca(2+) exchange were decreased by Cytomix-100. SR Ca(2+) pump (SERCA) (SR Ca(2+) ATPase) was not affected.
conclusionsProlonged exposure of ARVM to a mixture of LPS and inflammatory cytokines inhibits cell contractility. The effect is mediated by the inhibition of Ca(2+) influx via LTCC, and partially opposed by the inhibition of Na(+)/Ca(2+) exchange. Because both mechanisms are commonly seen in animal models of SIC, we conclude that prolonged challenge with Cytomix-100 of ARVM may represent an accurate in vitro model for SIC.
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