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

Identifieur interne : 000720 ( PubMed/Curation ); précédent : 000719; suivant : 000721

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

Auteurs : P J Sikes [États-Unis] ; P. Zhao ; D L Maass ; J W Horton

Source :

RBID : pubmed:11717236

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Abstract

In this study, (23)Na- and (31)P- 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. (23)Na-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 (31)P 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.

PubMed: 11717236

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<name sortKey="Sikes, P J" sort="Sikes, P J" uniqKey="Sikes P" first="P J" last="Sikes">P J Sikes</name>
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<nlm:affiliation>Department of Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9160, USA.</nlm:affiliation>
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<term>Acidosis (physiopathology)</term>
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<term>Burns (metabolism)</term>
<term>Burns (physiopathology)</term>
<term>Energy Metabolism</term>
<term>Hydrogen-Ion Concentration</term>
<term>Intracellular Membranes (metabolism)</term>
<term>Magnetic Resonance Spectroscopy</term>
<term>Male</term>
<term>Myocardial Contraction</term>
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<term>Phosphorus</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Sodium (metabolism)</term>
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<term>Acidose (physiopathologie)</term>
<term>Animaux</term>
<term>Brûlures (métabolisme)</term>
<term>Brûlures (physiopathologie)</term>
<term>Concentration en ions d'hydrogène</term>
<term>Contraction myocardique</term>
<term>Facteurs temps</term>
<term>Fonction ventriculaire gauche</term>
<term>Isotopes du sodium</term>
<term>Membranes intracellulaires (métabolisme)</term>
<term>Myocarde (métabolisme)</term>
<term>Mâle</term>
<term>Métabolisme énergétique</term>
<term>Phosphore</term>
<term>Rat Sprague-Dawley</term>
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<term>Sodium (métabolisme)</term>
<term>Spectrométrie de fluorescence</term>
<term>Spectroscopie par résonance magnétique</term>
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<term>Intracellular Membranes</term>
<term>Myocardium</term>
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<term>Brûlures</term>
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<term>Sodium</term>
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<term>Hydrogen-Ion Concentration</term>
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<term>Métabolisme énergétique</term>
<term>Phosphore</term>
<term>Rat Sprague-Dawley</term>
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<div type="abstract" xml:lang="en">In this study, (23)Na- and (31)P- 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. (23)Na-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 (31)P 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.</div>
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