Role of sodium/calcium exchange in the mechanism of myocardial stunning: Protective effect of reperfusion with high sodium solution

Hideo Kusuoka, Maria C Camilion de Hurtado, Eduardo Marban

Research output: Contribution to journalArticle

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]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.

Original languageEnglish (US)
Pages (from-to)240-248
Number of pages9
JournalJournal of the American College of Cardiology
Volume21
Issue number1
DOIs
StatePublished - 1993

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Myocardial Stunning
Reperfusion
Sodium
Calcium
Pressure
Osmolar Concentration
Phosphorus
Magnetic Resonance Spectroscopy
Phosphorus Compounds
Ferrets
Ventricular Pressure
Sucrose
Chlorides
Ischemia

ASJC Scopus subject areas

  • Nursing(all)

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Role of sodium/calcium exchange in the mechanism of myocardial stunning : Protective effect of reperfusion with high sodium solution. / Kusuoka, Hideo; de Hurtado, Maria C Camilion; Marban, Eduardo.

In: Journal of the American College of Cardiology, Vol. 21, No. 1, 1993, p. 240-248.

Research output: Contribution to journalArticle

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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]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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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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