ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Endotoxin impairs cardiac hemodynamics by affecting loading conditions but not by reducing cardiac inotropism.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Left ventricular systolic function evaluated by strain echocardiography and relationship with mortality in patients with severe sepsis or septic shock: a systematic review and meta-analysis.Critical care (London, England) · 2018Pooled it
- Transcranial photoacoustic imaging of indocyanine green J-aggregates reveals cerebral signal changes in lipopolysaccharide-induced systemic inflammation.Photoacoustics · 2026Article
- Amphiregulin attenuates sepsis-induced myocardial dysfunction by maintaining the localization of connexin43.Inflammation and regeneration · 2026Article
- Precision Profiling of Disease Progression in Murine Models of Sepsis and Septic Shock.International journal of molecular sciences · 2025Article
- Acute inflammation induced by the Escherichia coli lipopolysaccharide considerably increases the systemic and brain exposure of olanzapine after oral administration in mice.The international journal of neuropsychopharmacology · 2025Article
- The direct effect of lipopolysaccharide on an isolated heart is different from the effect on cardiac myocytesArchives of medical science : AMS · 2023Article
- The roles of the inhibitory autophagy regulator Rubicon in the heart: A new therapeutic target to prevent cardiac cell death.Experimental & molecular medicine · 2021Review
- LncRNA MIAT downregulates IL-1β, TNF-ɑ to suppress macrophage inflammation but is suppressed by ATP-induced NLRP3 inflammasome activation.Cell cycle (Georgetown, Tex.) · 2021Article
- Dynamic Arterial Elastance During Experimental Endotoxic Septic Shock: A Potential Marker of Cardiovascular Efficiency.Frontiers in physiology · 2020Article
- Transcriptomic effects of adenosine 2A receptor deletion in healthy and endotoxemic murine myocardium.Purinergic signalling · 2017Article
- Article
- Mitochondrial Impairment in Cerebrovascular Endothelial Cells is Involved in the Correlation between Body Temperature and Stroke Severity.Aging and disease · 2016Article
- The role of speckle tracking echocardiography in assessment of lipopolysaccharide-induced myocardial dysfunction in mice.Journal of thoracic disease · 2015Article
- Endotoxemia Induces IκBβ/NF-κB-Dependent Endothelin-1 Expression in Hepatic Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Tissue inflammation and nitric oxide-mediated alterations in cardiovascular function are major determinants of endotoxin-induced insulin resistance.Cardiovascular diabetology · 2015Article
- Quantification of microcirculatory blood flow: a sensitive and clinically relevant prognostic marker in murine models of sepsis.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Article
- Analysis of the severity and prognosis assessment of aged patients with community-acquired pneumonia: a retrospective study.Journal of thoracic disease · 2013Article
- Electrophilic nitro-fatty acids inhibit vascular inflammation by disrupting LPS-dependent TLR4 signalling in lipid rafts.Cardiovascular research · 2013Article
- Caspase-3 protects stressed organs against cell death.Molecular and cellular biology · 2012Article
- Lipopolysaccharide prolongs action potential duration in HL-1 mouse cardiomyocytes.American journal of physiology. Cell physiology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Acute myocardial dysfunction is a typical manifestation of septic shock. Experimentally, the administration of endotoxin [lipopolysacharride (LPS)] to laboratory animals is frequently used to study such dysfunction. However, a majority of studies used load-dependent indexes of cardiac function [including ejection fraction (EF) and maximal systolic pressure increment (dP/dt(max))], which do not directly explore cardiac inotropism. Therefore, we evaluated the direct effects of LPS on myocardial contractility, using left ventricular (LV) pressure-volume catheters in mice. Male BALB/c mice received an intraperitoneal injection of E. coli LPS (1, 5, 10, or 20 mg/kg). After 2, 6, or 20 h, cardiac function was analyzed in anesthetized, mechanically ventilated mice. All doses of LPS induced a significant drop in LV stroke volume and a trend toward reduced cardiac output after 6 h. Concomitantly, there was a significant decrease of LV preload (LV end-diastolic volume), with no apparent change in LV afterload (evaluated by effective arterial elastance and systemic vascular resistance). Load-dependent indexes of LV function were markedly reduced at 6 h, including EF, stroke work, and dP/dt(max). In contrast, there was no reduction of load-independent indexes of LV contractility, including end-systolic elastance (ejection phase measure of contractility) and the ratio dP/dt(max)/end-diastolic volume (isovolumic phase measure of contractility), the latter showing instead a significant increase after 6 h. All changes were transient, returning to baseline values after 20 h. Therefore, the alterations of cardiac function induced by LPS are entirely due to altered loading conditions, but not to reduced contractility, which may instead be slightly increased.
Indexed as
Identifiers
What OpenQuestion holds
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.