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Am J Physiol Heart Circ Physiol (March 13, 2003). doi:10.1152/ajpheart.00833.2002
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Submitted on September 23, 2002
Accepted on February 18, 2003

The Cardiac Effects of Burn Injury Complicated by Aspiration-Pneumonia-Induced Sepsis

Jean White1, James Thomas2, David L. Maass1, and Jureta W. Horton1*

1 Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas, USA
2 Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas, USA

* To whom correspondence should be addressed. E-mail: jureta.horton{at}utsouthwestern.edu.

INTRODUCTION: Early fluid resuscitation, anti-microbials, early excision and grafting have improved survival in the early postburn period; yet, a significant incidence of pneumonia-related sepsis occurs after burn injury, often progressing to multiple organ failure. Recent studies have suggested that this initial injury (burn injury) primes the subject, producing an exaggerated response to a second insult such as pneumonia-related sepsis. METHODS: We developed an experimental animal model which included a 3° burn over 40% total body surface area, followed by sepsis (intratracheal administration of S. pneumoniae, 4x106 CFU) which was produced either 48 or 72 hours after burn injury in adult male rats. Hearts harvested after either burn alone, sepsis alone, or burn plus sepsis were used to assess either contractile function (Langendorff) or cardiomyocyte secretion of TNF-{alpha}, IL-1{beta}, IL-6, and IL-10 (ELISA). Experimental groups included 1) sham (sham burn and no sepsis); 2) burn injury alone studied either 24, 48, or 72 hrs postburn; 3) pneumonia-related sepsis in the absence of burn injury; and 4) pneumonia-induced sepsis studied either 48 or 72 hrs after an initial burn injury. RESULTS: Burn injury alone (24 hours) or sepsis alone produced myocardial contractile defects and increases in pro- and anti-inflammatory cytokine secretion by cardiomyocytes. Sepsis which occurred 48 hrs postburn exacerbated the cardiac contractile defects seen with either burn alone or sepsis alone. Sepsis which occurred 72 hrs postburn produced contractile defects resembling those seen in either burn alone or sepsis alone. CONCLUSIONS: Our data suggest that burn injury primes the subject such that a second insult early in the postburn period produces significantly greater cardiac abnormalities than seen with either burn alone or sepsis alone.




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