Abstract
23Na nuclear magnetic resonance (NMR) spectroscopy was utilized to measure intracellular Na+ in perfused ferret hearts exposed to the shift reagent dysprosium triethylenetramine-hexa-acetic acid [Dy(TTHA)3-]. The intracellular Na+ signal was small under normal perfusion conditions; resolution was enhanced by using a Jump-Return NMR pulse protocol. During 20 min of total global ischemia at 30 degrees C, intracellular Na+ concentration ([Na+]i) increased steadily to a peak value fivefold greater than control. [Na+]i declined monotonically back to control levels within 9 min of reperfusion. In contrast, the mean contractile pressure only recovered to 54% of control levels. Thus major alterations in Na+ homeostasis occur during severe ischemia. [Na+] recovers rapidly during reperfusion and is therefore dissociated from the lingering postischemic depression of contractile function known as "stunning."
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