Document Detail


Myocardial inflammatory responses to sepsis complicated by previous burn injury.
MedLine Citation:
PMID:  15012863     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: It is generally accepted that an initial injury such as burn trauma alters immune function such that a second insult increases the morbidity and mortality over that observed with each individual insult. We have shown previously that either burn trauma or sepsis promotes cardiomyocyte secretion of TNF-alpha and IL-1beta, cytokines that have been shown to produce myocardial contractile dysfunction. This study determined whether a previous burn injury (given eight days prior to sepsis) (1) provides a preconditioning phenomenon, decreasing inflammatory responses to a second insult or (2) exacerbates inflammatory response observed with either injury alone.
METHODS: Anesthetized Sprague-Dawley rats were given either burn injury over 40% total body surface area, sepsis alone (intratracheal S. pneumoniae, 4 x 10(6) colony forming units) or sepsis eight days after burn; all rats received lactated Ringer's solution. Hearts harvested 24 h after onset of sepsis alone or sepsis plus eight-day burn were used to (1) isolate cardiomyocytes (collagenase) or (2) assess contractile function (Langendorff). Cardiomyocytes loaded with 2 microg/mL Fura-2AM or sodium-binding benzofuran isophthalate were used to measure intracellular calcium and sodium concentrations (Nikon inverted microscope, Grooney optics, InCyt Im2 Fluorescence Imaging System). Additional cardiomyocytes were used to measure myocyte-secreted TNFalpha, IL-1, IL-6, IL-10 (pg/ml, ELISA).
RESULTS: Either burn trauma alone or sepsis alone promoted TNF-alpha, IL-1beta, nitric oxide, IL6 and IL-10 secretion by cardiomyocytes (p < 0.05). Producing aspiration-related pneumonia eight days postburn produced myocardial pro- and anti-inflammatory responses and increased myocyte Ca2+/Na+ concentrations to a significantly greater degree than the responses observed after either insult alone.
CONCLUSIONS: A previous burn injury alters myocardial inflammatory responses, predisposing the burn-injured subject to exaggerated inflammation, which correlates with greater myocardial dysfunction.
Authors:
Jureta W Horton; David L Maass; Jean White; Billy Sanders
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Surgical infections     Volume:  4     ISSN:  1096-2964     ISO Abbreviation:  Surg Infect (Larchmt)     Publication Date:  2003  
Date Detail:
Created Date:  2004-03-11     Completed Date:  2004-05-20     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  9815642     Medline TA:  Surg Infect (Larchmt)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  363-77     Citation Subset:  IM    
Affiliation:
Department of Surgery, UT Southwestern Medical Center, Dallas, Texas 75390-9160, USA. jureta.horton@utsouthwestern.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Burns / immunology*,  physiopathology
Cytokines / secretion*
Disease Models, Animal
Male
Myocardial Contraction / physiology*
Myocytes, Cardiac / secretion*
Pneumonia, Pneumococcal / immunology*,  physiopathology
Random Allocation
Rats
Rats, Sprague-Dawley
Sepsis / immunology*,  physiopathology
Streptococcus pneumoniae
Time Factors
Grant Support
ID/Acronym/Agency:
R01 GM057054-05/GM/NIGMS NIH HHS; R01 GM57054-0IAI/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines
Comments/Corrections

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