| Myocardial inflammatory responses to sepsis complicated by previous burn injury. | |
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MedLine Citation:
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PMID: 15012863 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Jureta W Horton; David L Maass; Jean White; Billy Sanders |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Surgical infections Volume: 4 ISSN: 1096-2964 ISO Abbreviation: Surg Infect (Larchmt) Publication Date: 2003 |
Date Detail:
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Created Date: 2004-03-11 Completed Date: 2004-05-20 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 9815642 Medline TA: Surg Infect (Larchmt) Country: United States |
Other Details:
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Languages: eng Pagination: 363-77 Citation Subset: IM |
Affiliation:
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Department of Surgery, UT Southwestern Medical Center, Dallas, Texas 75390-9160, USA. jureta.horton@utsouthwestern.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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R01 GM057054-05/GM/NIGMS NIH HHS; R01 GM57054-0IAI/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cytokines |
| Comments/Corrections | |
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