title: Reducing susceptibility to bacteremia after experimental burn injury: a role for selective decontamination of the digestive tract.
abstract: We proposed that selective decontamination of the digestive tract (SDD) initiated after experimental burn injury would decrease myocardial inflammation and dysfunction after a second insult such as septic challenge. Rats were divided into eight experimental groups. Groups included sham burn plus sham sepsis, burn alone, sepsis alone, and burn plus sepsis given either water by oral gavage for 5 days after burn (or sham burn) or given oral antibiotics (polymyxin E, 15 mg; tobramycin, 6 mg; 5-flucytosin, 100 mg given by oral gavage, 2x daily for 5 days after burn or sham burn). Cardiac function and inflammation were studied 24 h after septic challenge. In the absence of SDD, burn alone, sepsis alone, or burn plus septic challenge promoted cardiac myocyte secretion of TNF-alpha (burn, 174+/-11; sepsis, 269+/-19; burn+sepsis, 453+/-14 pg/ml), IL-1beta (burn, 35+/-2; sepsis, 29+/-1; burn+sepsis, 48+/-7 pg/ml), and IL-6 (burn, 143+/-18; sepsis, 116+/-3; burn+sepsis, 248+/-12 pg/ml) compared with values measured in sham (TNF-alpha, 3+/-1; IL-1beta, 1+/-0.4; IL-6, 6+/-1.5 pg/ml) (P<0.05). Impaired ventricular contraction and relaxation responses were evident in the absence of SDD [burn+sepsis: left ventricular pressure (LVP), 65+/-4 mmHg; rate of LVP rise (+dP/dt), 1,320+/-131 mmHg/s compared with values measured in sham: LVP, 96+/-4 mmHg; +dP/dt, 2,095+/-99 mmHg/s, P<0.05]. SDD treatment of experimental burn attenuated septic challenge-related inflammatory responses and improved myocardial contractile responses, producing cardiac TNF-alpha, IL-1beta, and IL-6 levels, LVP, +dP/dt, and rate of LVP fall (-dP/dt) values that were significantly better (P<0.05) than values measured in burn plus sepsis in the absence of SDD. This work confirms that endogenous gut organisms contribute to sensitivity to subsequent infectious challenge.
authors.affiliation: Department of Surgery, University of Texas Southwestern Medical Center, 5325 Harry Hines Blvd., Dallas, TX 75390, USA. jureta.horton@utsouthwestern.edu
authors.forename: Jureta W
authors.initials: JW
authors.lastname: Horton
authors.forename: David L
authors.initials: DL
authors.lastname: Maass
authors.forename: Jean
authors.initials: J
authors.lastname: White
authors.forename: Joseph P
authors.initials: JP
authors.lastname: Minei
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000008:administration & dosage*; D016470:Bacteremia / Q000209:etiology / Q000276:immunology* / Q000382:microbiology / Q000517:prevention & control*; D004195:Disease Models, Animal; D041981:Gastrointestinal Tract / Q000187:drug effects* / Q000276:immunology / Q000382:microbiology*; D008297:Male; D009205:Myocarditis / Q000209:etiology / Q000276:immunology* / Q000382:microbiology / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000900:Anti-Bacterial Agents