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Am J Physiol Heart Circ Physiol 290: H1642-H1650, 2006. First published November 18, 2005; doi:10.1152/ajpheart.00586.2005
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Hypertonic saline dextran after burn injury decreases inflammatory cytokine responses to subsequent pneumonia-related sepsis

Jureta W. Horton, David L. Maass, and D. Jean White

Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas

Submitted 2 June 2005 ; accepted in final form 3 November 2005

The present study examined the hypothesis that hypertonic saline dextran (HSD), given after an initial insult, attenuates exaggerated inflammation that occurs with a second insult. Adult rats (n = 15 per group) were divided into groups 1 (sham burn), 2 [40% total body surface area burn + 4 ml/kg isotonic saline (IS) + 4 ml·kg–1·% burn–1 lactated Ringer solution (LR)], and 3 (burn + 4 ml/kg HSD + LR), all studied 24 h after burns. Groups 4 (sham burn), 5 (burn + IS + LR), and 6 (burns + HSD + LR) received intratracheal (IT) vehicle 7 days after burns; groups 7 (burn + IS + LR) and 8 (burn + HSD + LR) received IT Streptococcus pneumoniae (4 x 106 colony-forming units) 7 days after burn. Groups 4–8 were studied 8 days after burn and 24 h after IT septic challenge. When compared with sham burn, contractile defects occurred 24 h after burn in IS-treated but not HSD-treated burns. Cardiac inflammatory responses (pg/ml TNF-{alpha}) were evident with IS (170 ± 10) but not HSD (45 ± 5) treatment vs. sham treatment (80 ± 15). Pneumonia-related sepsis 8 days after IS-treated burns (group 7) exacerbated TNF-{alpha} responses/contractile dysfunction vs. IS-treated burns in the absence of sepsis (P < 0.05). Sepsis that occurred after HSD-treated burns (group 8) had less myocyte TNF-{alpha} secretion/better contractile function than IS-treated burns given septic challenge (group 7, P < 0.05). We conclude that an initial burn injury exacerbates myocardial inflammation/dysfunction occurring with a second insult; giving HSD after the initial insult attenuates myocardial inflammation/dysfunction associated with a second hit, suggesting that HSD reduces postinjury risk for infectious complications.

rat model; Langendorff perfusion; burn complicated by sepsis; cardiac myocytes; tumor necrosis factor-{alpha}; interleukin-1beta; interleukin-6



Address for reprint requests and other correspondence: J. W. Horton, Dept. of Surgery, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9160 (e-mail: jureta.horton{at}utsouthwestern.edu)




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