TY - JOUR
T1 - Role of sodium/calcium exchange in the mechanism of myocardial stunning
T2 - Protective effect of reperfusion with high sodium solution
AU - Kusuoka, Hideo
AU - de Hurtado, Maria C.Camilion
AU - Marban, Eduardo
PY - 1993/1
Y1 - 1993/1
N2 - 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]0 solution ([Na]0 = 268 mmol/liter) during the initial 5 min, followed by a gradual decrease of [Na]0 to the standard level over 25 min (the high [Na]0 group, 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]0 reperfusion 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]0 reperfusion protects against stunning, supporting the concept that Na+ Ca2+ exchange plays an important role in the mechanism of stunned myocardium.
AB - 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]0 solution ([Na]0 = 268 mmol/liter) during the initial 5 min, followed by a gradual decrease of [Na]0 to the standard level over 25 min (the high [Na]0 group, 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]0 reperfusion 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]0 reperfusion protects against stunning, supporting the concept that Na+ Ca2+ exchange plays an important role in the mechanism of stunned myocardium.
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U2 - 10.1016/0735-1097(93)90743-K
DO - 10.1016/0735-1097(93)90743-K
M3 - Article
C2 - 8417067
AN - SCOPUS:0027518453
VL - 21
SP - 240
EP - 248
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
SN - 0735-1097
IS - 1
ER -