Reducing susceptibility to bacteremia after experimental burn injury

A role for selective decontamination of the digestive tract

Jureta W. Horton, David L. Maass, Jean White, Joseph P. Minei

Research output: Contribution to journalArticle

10 Citations (Scopus)

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-α (burn, 174 ± 11; sepsis, 269 ± 19; burn ± sepsis, 453 ± 14 pg/ml), IL-1β (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-α, 3 ± 1; IL-1β, 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-α, IL-1β, 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.

Original languageEnglish (US)
Pages (from-to)2207-2216
Number of pages10
JournalJournal of Applied Physiology
Volume102
Issue number6
DOIs
StatePublished - Jun 2007

Fingerprint

Decontamination
Bacteremia
Gastrointestinal Tract
Sepsis
Wounds and Injuries
Ventricular Pressure
Interleukin-1
Interleukin-6
Inflammation
Colistin
Tobramycin
Cardiac Myocytes

Keywords

  • Adult Sprague-Dawley rats
  • Inflammatory cytokines
  • Intratracheal bacterial challenge
  • Isolated cardiac myocytes
  • Oral antibiotics
  • Postburn cardiac function
  • Streptococcus pneumoniae

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Reducing susceptibility to bacteremia after experimental burn injury : A role for selective decontamination of the digestive tract. / Horton, Jureta W.; Maass, David L.; White, Jean; Minei, Joseph P.

In: Journal of Applied Physiology, Vol. 102, No. 6, 06.2007, p. 2207-2216.

Research output: Contribution to journalArticle

@article{6a57469c99e54896a35c5bc558a6a4e9,
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-α (burn, 174 ± 11; sepsis, 269 ± 19; burn ± sepsis, 453 ± 14 pg/ml), IL-1β (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-α, 3 ± 1; IL-1β, 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-α, IL-1β, 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.",
keywords = "Adult Sprague-Dawley rats, Inflammatory cytokines, Intratracheal bacterial challenge, Isolated cardiac myocytes, Oral antibiotics, Postburn cardiac function, Streptococcus pneumoniae",
author = "Horton, {Jureta W.} and Maass, {David L.} and Jean White and Minei, {Joseph P.}",
year = "2007",
month = "6",
doi = "10.1152/japplphysiol.01365.2005",
language = "English (US)",
volume = "102",
pages = "2207--2216",
journal = "Journal of Applied Physiology",
issn = "0161-7567",
publisher = "American Physiological Society",
number = "6",

}

TY - JOUR

T1 - Reducing susceptibility to bacteremia after experimental burn injury

T2 - A role for selective decontamination of the digestive tract

AU - Horton, Jureta W.

AU - Maass, David L.

AU - White, Jean

AU - Minei, Joseph P.

PY - 2007/6

Y1 - 2007/6

N2 - 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-α (burn, 174 ± 11; sepsis, 269 ± 19; burn ± sepsis, 453 ± 14 pg/ml), IL-1β (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-α, 3 ± 1; IL-1β, 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-α, IL-1β, 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.

AB - 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-α (burn, 174 ± 11; sepsis, 269 ± 19; burn ± sepsis, 453 ± 14 pg/ml), IL-1β (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-α, 3 ± 1; IL-1β, 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-α, IL-1β, 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.

KW - Adult Sprague-Dawley rats

KW - Inflammatory cytokines

KW - Intratracheal bacterial challenge

KW - Isolated cardiac myocytes

KW - Oral antibiotics

KW - Postburn cardiac function

KW - Streptococcus pneumoniae

UR - http://www.scopus.com/inward/record.url?scp=34447530821&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34447530821&partnerID=8YFLogxK

U2 - 10.1152/japplphysiol.01365.2005

DO - 10.1152/japplphysiol.01365.2005

M3 - Article

VL - 102

SP - 2207

EP - 2216

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 0161-7567

IS - 6

ER -