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

Sikes, Patricia J., Piyu Zhao, David L. Maass, and Jureta W. Horton. Time course of myocardial sodium accumulation after burn trauma: a 31Pand 23Na-NMR study. J Appl Physiol 91: 2695–2702, 2001.—In this study, 23Naand 31Pnuclear 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 zkg21 z%21 burn. 23Na-NMR spectroscopy monitored myocardial intracellular Na using the paramagnetic shift reagent thulium 1,4,7,10-tetraazacyclododecane1,4,7,10-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.