Journal of Applied Physiology
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J Appl Physiol 91: 2695-2702, 2001;
8750-7587/01 $5.00
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Vol. 91, Issue 6, 2695-2702, December 2001

Time course of myocardial sodium accumulation after burn trauma: a 31P- and 23Na-NMR study

Patricia J. Sikes1, Piyu Zhao2, David L. Maass1, and Jureta W. Horton1

Departments of 1 Surgery and 2 Radiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9160

In this study, 23Na- and 31P- nuclear magnetic resonance (NMR) spectra were examined in perfused rat hearts harvested 1, 2, 4, and 24 h after 40% total body surface area burn trauma and lactated Ringer resuscitation, 4 ml · kg-1 · %-1 burn. 23Na-NMR spectroscopy monitored myocardial intracellular Na+ using the paramagnetic shift reagent thulium 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetra(methylenephosphonic acid). Left ventricular function, cardiac high-energy phosphates (ATP/PCr), and myocyte intracellular pH were studied by using 31P NMR spectroscopy to examine the hypothesis that burn-mediated acidification of cardiomyocytes contributes to subsequent Na+ accumulation by this cell population. Intracellular Na+ accumulation was confirmed by sodium-binding benzofuran isophthalate loading and fluorescence spectroscopy in cardiomyocytes isolated 1, 2, 4, 8, 12, 18, and 24 h postburn. This myocyte Na+ accumulation as early as 2 h postburn occurred despite no changes in cardiac ATP/PCr and intracellular pH. Left ventricular function progressively decreased after burn trauma. Cardiomyocyte Na+ accumulation paralleled cardiac contractile dysfunction, suggesting that myocardial Na+ overload contributes, in part, to the progressive postburn decrease in ventricular performance.

nuclear magnetic resonance spectroscopy; cardiomyocyte loading of the fluorescent indicator sodium-binding benzofuran isophthalate; ventricular contraction-relaxation assessed by Langendorff perfusion; myocardial acidosis (intracellular pH); myocardial high-energy phosphate stores


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