Selective decontamination of the digestive tract attenuated the myocardial inflammation and dysfunction that occur with burn injury
| Autor: | Jing Tan, David L. Maass, D. Jean White, Jureta W. Horton, James A. Thomas |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Male
Burn injury Pathology medicine.medical_specialty Physiology medicine.drug_class medicine.medical_treatment Antibiotics Inflammation Rats Sprague-Dawley Contractility Physiology (medical) medicine Animals Myocytes Cardiac Interleukin 6 Chemotherapy biology business.industry Sodium NF-kappa B Interleukin Heart Myocardial Contraction Anti-Bacterial Agents Rats Gastrointestinal Tract Myocarditis Cytokine biology.protein Cytokines Calcium Inflammation Mediators medicine.symptom Burns Cardiology and Cardiovascular Medicine business Signal Transduction |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 287:H2241-H2251 |
| ISSN: | 1522-1539 0363-6135 |
| DOI: | 10.1152/ajpheart.00390.2004 |
| Popis: | This study examined the effects of oral antibiotics to selectively decontaminate the digestive tract (SDD) on postburn myocardial signaling, inflammation, and function. We hypothesized that antibiotic therapy to eliminate pathogens from the gastrointestinal (GI) tract would reduce myocardial inflammatory responses and improve postburn myocardial performance. Sprague-Dawley rats received polymyxin E (15 mg), tobramycin (6 mg), and 5-flucytosin (100 mg) by oral gavage twice daily for 3 days preburn and 24 h postburn. Experimental groups included 1) sham burn given vehicle (3 ml water), 2) sham plus SDD, 3) burn over 40% total body surface area (TBSA) plus SDD, and 4) burn over 40% TBSA given vehicle. All burns received lactated Ringer solution (4 mg·kg−1·%burn−1); myocardial signaling (PKCε/p38 MAPK/NF-κB) was studied 2, 4, and 24 h postburn; and cytokine secretion (systemic and myocyte secreted cytokines, ELISA) and cardiac function were examined 24 h postburn. Vehicle-treated burn injury increased myocardial PKCε/p38 MAPK expression, promoted NF-κB nuclear translocation, promoted TNF-α, IL-1β, IL-6, and IL-10 secretion, and impaired myocardial function. SDD attenuated burn-related proinflammatory myocardial signaling, cytokine secretion, and myocardial contractile defects. Our data suggest that burn-related loss of GI barrier function and translocation of microbial products serve as upstream mediators of postburn myocardial inflammatory signaling and dysfunction. |
| Databáze: | OpenAIRE |
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