Document Detail

TLR4 inactivation and rBPI(21) block burn-induced myocardial contractile dysfunction.
MedLine Citation:
PMID:  12234819     Owner:  NLM     Status:  MEDLINE    
Both large burns and severe gram-negative sepsis are associated with acute myocardial contractile dysfunction. Because others have reported that burn injury may be followed by transient endotoxemia, we hypothesized that bacterial endotoxin induces contractile impairment after burn trauma. We tested this hypothesis in two rodent models. In each model, postburn myocardial contractility was assessed using Langendorff preparations of excised hearts. In the first model, mice expressing either a mutant form of or no Toll-like receptor 4 (TLR4), a critical element of the mammalian endotoxin receptor, were resistant to postburn myocardial contractile dysfunction. In the second model, starting 30 min or 4 h after burn injury, rats were infused with recombinant bactericidal/permeability-increasing protein (rBPI(21)), a protein that binds and neutralizes endotoxin. Hearts from rBPI(21)-treated animals were completely protected from postburn contractile impairment. Because burn-induced contractile dysfunction can be prevented either by blocking signaling through the endotoxin receptor or by neutralizing circulating LPS, bacterial endotoxin may contribute to impaired myocardial contractility after burn injury.
James A Thomas; May F Tsen; D Jean White; Jureta W Horton
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2002-06-13
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  283     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2002 Oct 
Date Detail:
Created Date:  2002-09-17     Completed Date:  2002-10-17     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1645-55     Citation Subset:  IM    
Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75390, USA.
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MeSH Terms
Antimicrobial Cationic Peptides
Blood Proteins / genetics*
Burns / physiopathology*
Cardiac Volume / physiology
Coronary Circulation / physiology
Disease Models, Animal
Drosophila Proteins*
Endotoxemia / physiopathology
Lipopolysaccharides / pharmacology
Membrane Glycoproteins / genetics*
Membrane Proteins*
Mice, Inbred C3H
Mice, Inbred C57BL
Mice, Mutant Strains
Myocardial Contraction / physiology*
Rats, Sprague-Dawley
Receptors, Cell Surface / genetics*
Signal Transduction / physiology
Toll-Like Receptor 4
Toll-Like Receptors
Grant Support
5-P50-GM-21681-37/GM/NIGMS NIH HHS
Reg. No./Substance:
0/Antimicrobial Cationic Peptides; 0/Blood Proteins; 0/Drosophila Proteins; 0/Lipopolysaccharides; 0/Membrane Glycoproteins; 0/Membrane Proteins; 0/Receptors, Cell Surface; 0/Tlr4 protein, rat; 0/Toll-Like Receptor 4; 0/Toll-Like Receptors; 0/bactericidal permeability increasing protein

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

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