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Am J Physiol Heart Circ Physiol 280: H1591-H1601, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 4, H1591-H1601, April 2001

Hypertonic saline-dextran suppresses burn-related cytokine secretion by cardiomyocytes

Jureta W. Horton, David L. Maass, Jean White, and Billy Sanders

Department of Surgery, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-9160

Whereas hypertonic saline-dextran (HSD, 7.5% NaCl in 6% D70) improves cardiac contractile function after burn trauma, the mechanisms of HSD-related cardioprotection remain unclear. We recently showed that cardiomyocytes secrete tumor necrosis factor-alpha (TNF-alpha ), a response that was enhanced by burn trauma. This study addressed the question: does HSD modulate cardiac contraction/relaxation by altering cardiomyocyte TNF-alpha secretion? Wistar-Furth rats (325 g) were given a burn injury over 40% of the total body surface area and were then randomized to receive a bolus of either isotonic saline or HSD (4 ml/kg, n = 14 rats/group). Sham burn rats were given either isotonic saline or HSD (n = 14 rats/group) to provide appropriate controls for the two burn groups. Hearts were isolated 24 h postburn for either Langendorff perfusion (n = 8 hearts/group) or to prepare cardiomyocytes (n = 6 hearts/group). Myocytes were stimulated with lipopolysaccharide (LPS) (0, 10, 25, or 50 µg for 18 h) to measure cytokine secretion. Burn trauma increased myocyte TNF-alpha and interleukin-1beta and -6 secretion, exacerbated cytokine response to LPS stimulus, and impaired cardiac contraction. HSD treatment of burns decreased cardiomyocyte cytokine secretion, decreased responsiveness to LPS challenge with regard to cytokine secretion, and improved ventricular function. These data suggest that HSD mediates cardioprotection after burn trauma, in part, by downregulating cardiomyocyte secretion of inflammatory cytokines.

cardiac contractile function; rat model of burn trauma; tumor necrosis factor-alpha ; Langendorff perfusion


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