Cardiac effects of burn injury complicated by aspiration pneumonia-induced sepsis.
Early fluid resuscitation, antimicrobials, early excision, and grafting have improved survival in the early postburn period; however, 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. We developed an experimental animal model that included a third-degree burn over 40% of the total body surface area, followed by sepsis (intratracheal administration of Streptococcus pneumoniae, 4 x 106 colony-forming unit), which was produced either 48 or 72 h 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 tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, and IL-10 (ELISA). Experimental groups included the following: 1). sham (sham burn and no sepsis); 2). burn injury alone studied either 24, 48, or 72 h postburn; 3). pneumonia-related sepsis in the absence of burn injury; and 4). pneumonia-induced sepsis studied either 48 or 72 h after an initial burn injury. Burn injury alone (24 h) or sepsis alone produced myocardial contractile defects and increases in pro- and anti-inflammatory cytokine secretion by cardiomyocytes. Sepsis that occurred 48 h postburn exacerbated the cardiac contractile defects seen with either burn alone or sepsis alone. Sepsis that occurred 72 h postburn produced contractile defects resembling those seen in either burn alone or sepsis alone. In conclusion, 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 those seen with either burn alone or sepsis alone.
White
Jean
J
Department of Surgery, University of Texas Southwestern Medical Center, Dallas, TX 75390-9160, USA.
Thomas
James
J
Maass
David L
DL
Horton
Jureta W
JW
D000818:Animals; D002056:Burns / Q000150:complications* / Q000382:microbiology / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism; D006328:Cardiac Catheterization; D002469:Cell Separation; D006321:Heart / Q000382:microbiology / Q000503:physiopathology*; D066298:In Vitro Techniques; D007375:Interleukin-1 / Q000096:biosynthesis; D016753:Interleukin-10 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D011008:Pneumococcal Infections / Q000150:complications / Q000382:microbiology / Q000503:physiopathology; D011015:Pneumonia, Aspiration / Q000150:complications* / Q000382:microbiology / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000150:complications* / Q000382:microbiology / Q000503:physiopathology*; D012964:Sodium / Q000378:metabolism; D013296:Streptococcus pneumoniae; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D016277:Ventricular Function, Left / Q000502:physiology
D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D012964:Sodium; D002118:Calcium