Abstract
Objectives. This study was conducted to elucidate the role of sodium/calcium (Na+/Ca2+) exchange in the mechanism of myocardial stunning.Background. Cellular Ca2+overload mediated by Na+/Ca2+exchange during reperfusion has been proposed as a mechanism for myocardial stunning. Because no specific pharmacologic inhibitors of the exchanger are available, we increased extracellular sodium concentration ([Na]0) during the early phase of reperfusion to decrease the driving force for Ca2+influx through the pathway.Methods. Isovolumetric left ventricular pressure and phosphorus-31 nuclear magnetic resonance spectra were measured in isolated perfused ferret hearts. Hearts were reperfused with different solutions after 15 min of total global ischemia at 37 °C.Results. Hearts reperfused with standard solution ([Na]0= 140 mmol/liter; the stunned hearts, n = 8) showed only 69 ± 3% (mean ± SEM) recovery of developed pressure relative to preischemic control developed pressure, In contrast, hearts reperfused with a high [Na]0solution ([Na]0= 268 mmol/liter) during the initial 5 min, followed by a gradual decrease of [Na]0to the standard level over 25 min (the high [Na]0group, n = 8) showed significantly better recovery of developed pressure (85 ± 2%, p < 0.05 vs. the stunned hearts). in contrast, reperfusion with solutions in which the additional Na was substituted either by 256 mmol/liter sucrose or 128 mmol/liter chollne chloride did not improve functional recovery, indicating that the beneficial effects of high [Na]0reperfusion are not due to either high ionic strength or high osmolarity. Phosphorus-31 nuclear magnetic resonance spectra showed no correlation between functional recovery and intramyocardial contents of phosphorus compounds or pH.Conclusions. High [Na]0reperfusion protects against stunning, supporting the concept that Na+/Ca2+exchange plays an important role in the mechanism of stunned myocardium.
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