Document Detail


Lipopolysaccharide and sepsis-associated myocardial dysfunction.
MedLine Citation:
PMID:  21378563     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Tara M Balija; Stephen F Lowry
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Current opinion in infectious diseases     Volume:  24     ISSN:  1473-6527     ISO Abbreviation:  Curr. Opin. Infect. Dis.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-04-22     Completed Date:  2011-08-02     Revised Date:  2012-01-31    
Medline Journal Info:
Nlm Unique ID:  8809878     Medline TA:  Curr Opin Infect Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  248-53     Citation Subset:  IM    
Affiliation:
Department of Surgery, University of Medicine and Dentistry - Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomyopathies / chemically induced*,  immunology*
Humans
Lipopolysaccharides / immunology*,  toxicity*
Oxidative Stress
Sepsis / immunology*,  pathology*
Chemical
Reg. No./Substance:
0/Lipopolysaccharides

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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