| Lipopolysaccharide and sepsis-associated myocardial dysfunction. | |
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MedLine Citation:
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PMID: 21378563 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE OF REVIEW: Myocardial dysfunction in sepsis demonstrates acute reduction in left-ventricular function that is potentially reversible yet also associated with increased mortality. The purpose of this review is to discuss the most recent advances in the current knowledge regarding the pathophysiological mechanisms of septic cardiomyopathy. RECENT FINDINGS: There are numerous candidate pathophysiologic mechanisms for the induction of myocardial dysfunction in sepsis. Sarcolemmal and myofibrillar damage to septic rat cardiomyocytes has been observed, and is likely related to oxidative stress. In a septic chimeric murine model, wild-type mice had decreased cardiac function and increased myocardial TNF-α and IL-6 levels whereas TLR-4 knockout mice had attenuated responses to lipopolysaccharide challenge; thus contributing to the increasing evidence for TLR-4's role in the myocardial inflammatory response to lipopolysaccharide. A similar finding regarding endothelial cell NF-κβ signaling inhibition was found using knockout mice. SUMMARY: Septic cardiomyopathy is a significant morbid component of severe sepsis and septic shock. Further research into reducing cardiomyocyte damage via oxidative stress, reducing pro-inflammatory responses induced by TLR-4/NF-κβ signaling, decreasing mitochondrial dysfunction, and improving cellular respiration thereby decreasing apoptosis are examples of areas that may be future therapeutic targets. |
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Authors:
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Tara M Balija; Stephen F Lowry |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Current opinion in infectious diseases Volume: 24 ISSN: 1473-6527 ISO Abbreviation: Curr. Opin. Infect. Dis. Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-04-22 Completed Date: 2011-08-02 Revised Date: 2012-01-31 |
Medline Journal Info:
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Nlm Unique ID: 8809878 Medline TA: Curr Opin Infect Dis Country: United States |
Other Details:
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Languages: eng Pagination: 248-53 Citation Subset: IM |
Affiliation:
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Department of Surgery, University of Medicine and Dentistry - Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cardiomyopathies / chemically induced*, immunology* Humans Lipopolysaccharides / immunology*, toxicity* Oxidative Stress Sepsis / immunology*, pathology* |
| Chemical | |
Reg. No./Substance:
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0/Lipopolysaccharides |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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