Time course of myocardial sodium accumulation after burn trauma: a³¹P- and²³Na-NMR study

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.

Estrogen-provided cardiac protection following burn trauma is mediated through a reduction in mitochondria-derived DAMPs

“…Our lab established a rodent burn injury animal model to study this pathological condition (50). Our studies have shown that burn-induced cardiac dysfunction is associated with systemic and myocardial inflammation (5,54), abnormal iron homeostasis (4,55,63,76,83), and metabolism disorders (86,94). These findings in the rodent model are consistent with clinical observations (41,45,51,59).…”

Caspase inhibition reduces cardiac myocyte dyshomeostasis and improves cardiac contractile function after major burn injury

“…Hearts were harvested through a midline thoracotomy, and a cannula placed in the aorta was used to perfuse the coronary arteries (Krebs-Henseleit bicarbonate buffer) with a Langendorff approach. The hearts were perfused in a water-jacketed reservoir located in the bore of the NMR magnet (37,38,42). The hearts were suspended in a 20-mm OD magnetic resonance spectroscopy tube with a microtube holding 50 l of 1.3 mM NaCl and 3.3 mM Dy(DOTP)…”

“…The shift reagent Tm(DOTP) 5 was used to separate intra-and extracellular 23 Na signal in the isolated heart. A Varian INOVA 300 spectrometer equipped with an Oxford 4.2 T vertical-bore superconducting magnet with a Bruker 20-mm BB probe was used, tunable to either 23 Na or 31 P. The resonance areas were determined using NUTS (NMR Utility Transform Software 2D version; Acorn, NMR, 1996) (37,38,42).…”

“Systemic apoptotic response” after thermal burns

“…Cardiomyocyte calcium and sodium are affected through changes in calcium transporter expression and, in part, via reverse mode function of the sodium/calcium exchanger and via L-type channels. These effects are likely to contribute to cardiomyocyte calcium and sodium loading resulting in altered myocardial performance [90,[95][96][97].…”