Effects of low extracellular sodium concentration on reperfusion induced arrhythmias

Changes in the myocardial sodium, potassium and calcium contents in isolated Guinea pig hearts

A. Tósaki, Matyas Koltai, Pierre Braquet

Research output: Contribution to journalReview article

15 Citations (Scopus)

Abstract

Isolated Guinea pig hearts subjected to global ischaemia were used to investigate whether low extracellular Na+ exerts an anti-arrhythmic action against reperfusion arrhythmias, and the effects of extracellular Na+ manipulation upon myocardial ion contents (Na+, K+ and Ca2+) during ischaemia and reperfusion were studied. Using an optimal concentration of 144 mmol·litre-1 of extracellular Na+, hearts were subjected to 10, 20, 25, 30 or 40 min of global ischaemia followed by 25 min reperfusion. A bell shaped curve was obtained such that with increasing durations of ischaemia from 20 to 30 min there was an increasing incidence of reperfusion arrhythmias. Beyond this optimum (at which 100% exhibited reperfusion induced ventricular fibrillation and tachycardia) there was a decline in the susceptibility of the hearts to arrhythmias. Low extracellular Na+ was given 5 min prior to the global ischaemia and maintained during reperfusion. With extracellular Na+ of 24, 54, 84 and 114 mmol·litre-1, reperfusion induced ventricular fibrillation and tachycardia were reduced from their control incidence of 91% and 100% to 8% (p<0.001) and 17% (p<0.001), 17% (p<0.01) and 17% (p<0.001), 41% (p<0.05) and 50% (p<0.05), and 91% and 91%, respectively. Both ischaemia induced Na+ gain and K+ loss were inhibited by low extracellular Na+ (24 mmol·litre-1). During reperfusion, myocardial Na+ was further increased in the control group and this value was lower in the low extracellular Na+ group. In control hearts, myocardial K+ was suddenly increased during the first 5 min of reperfusion, then continuously decreased until the end of reperfusion. Low extracellular Na+reduced the sudden increase of myocardial K+ in the first few minutes of reperfusion, and inhibited its decline in the later course of reperfusion. Ischaemia induced a moderate accumulation of myocardial Ca2+ only, but there was a steep increase from the 5th min of reperfusion, and low extracellular Na+also prevented this increase.The results obtained described time dependent changes in myocardial ion contents in the course of reperfusion and indicate the beneficial effect of low extracellular Na+ against reperfusion arrhythmias.

Original languageEnglish
Pages (from-to)993-1000
Number of pages8
JournalCardiovascular Research
Volume23
Issue number12
DOIs
Publication statusPublished - Jan 1 1989

Fingerprint

Reperfusion
Cardiac Arrhythmias
Potassium
Guinea Pigs
Sodium
Calcium
Ischemia
Ventricular Fibrillation
Ventricular Tachycardia
Ions
Anti-Arrhythmia Agents
Incidence

Keywords

  • Extracellular sodium
  • Guinea pig
  • Myocardial ion contents
  • Reperfusion arrhythmias

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Effects of low extracellular sodium concentration on reperfusion induced arrhythmias : Changes in the myocardial sodium, potassium and calcium contents in isolated Guinea pig hearts. / Tósaki, A.; Koltai, Matyas; Braquet, Pierre.

In: Cardiovascular Research, Vol. 23, No. 12, 01.01.1989, p. 993-1000.

Research output: Contribution to journalReview article

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abstract = "Isolated Guinea pig hearts subjected to global ischaemia were used to investigate whether low extracellular Na+ exerts an anti-arrhythmic action against reperfusion arrhythmias, and the effects of extracellular Na+ manipulation upon myocardial ion contents (Na+, K+ and Ca2+) during ischaemia and reperfusion were studied. Using an optimal concentration of 144 mmol·litre-1 of extracellular Na+, hearts were subjected to 10, 20, 25, 30 or 40 min of global ischaemia followed by 25 min reperfusion. A bell shaped curve was obtained such that with increasing durations of ischaemia from 20 to 30 min there was an increasing incidence of reperfusion arrhythmias. Beyond this optimum (at which 100{\%} exhibited reperfusion induced ventricular fibrillation and tachycardia) there was a decline in the susceptibility of the hearts to arrhythmias. Low extracellular Na+ was given 5 min prior to the global ischaemia and maintained during reperfusion. With extracellular Na+ of 24, 54, 84 and 114 mmol·litre-1, reperfusion induced ventricular fibrillation and tachycardia were reduced from their control incidence of 91{\%} and 100{\%} to 8{\%} (p<0.001) and 17{\%} (p<0.001), 17{\%} (p<0.01) and 17{\%} (p<0.001), 41{\%} (p<0.05) and 50{\%} (p<0.05), and 91{\%} and 91{\%}, respectively. Both ischaemia induced Na+ gain and K+ loss were inhibited by low extracellular Na+ (24 mmol·litre-1). During reperfusion, myocardial Na+ was further increased in the control group and this value was lower in the low extracellular Na+ group. In control hearts, myocardial K+ was suddenly increased during the first 5 min of reperfusion, then continuously decreased until the end of reperfusion. Low extracellular Na+reduced the sudden increase of myocardial K+ in the first few minutes of reperfusion, and inhibited its decline in the later course of reperfusion. Ischaemia induced a moderate accumulation of myocardial Ca2+ only, but there was a steep increase from the 5th min of reperfusion, and low extracellular Na+also prevented this increase.The results obtained described time dependent changes in myocardial ion contents in the course of reperfusion and indicate the beneficial effect of low extracellular Na+ against reperfusion arrhythmias.",
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N2 - Isolated Guinea pig hearts subjected to global ischaemia were used to investigate whether low extracellular Na+ exerts an anti-arrhythmic action against reperfusion arrhythmias, and the effects of extracellular Na+ manipulation upon myocardial ion contents (Na+, K+ and Ca2+) during ischaemia and reperfusion were studied. Using an optimal concentration of 144 mmol·litre-1 of extracellular Na+, hearts were subjected to 10, 20, 25, 30 or 40 min of global ischaemia followed by 25 min reperfusion. A bell shaped curve was obtained such that with increasing durations of ischaemia from 20 to 30 min there was an increasing incidence of reperfusion arrhythmias. Beyond this optimum (at which 100% exhibited reperfusion induced ventricular fibrillation and tachycardia) there was a decline in the susceptibility of the hearts to arrhythmias. Low extracellular Na+ was given 5 min prior to the global ischaemia and maintained during reperfusion. With extracellular Na+ of 24, 54, 84 and 114 mmol·litre-1, reperfusion induced ventricular fibrillation and tachycardia were reduced from their control incidence of 91% and 100% to 8% (p<0.001) and 17% (p<0.001), 17% (p<0.01) and 17% (p<0.001), 41% (p<0.05) and 50% (p<0.05), and 91% and 91%, respectively. Both ischaemia induced Na+ gain and K+ loss were inhibited by low extracellular Na+ (24 mmol·litre-1). During reperfusion, myocardial Na+ was further increased in the control group and this value was lower in the low extracellular Na+ group. In control hearts, myocardial K+ was suddenly increased during the first 5 min of reperfusion, then continuously decreased until the end of reperfusion. Low extracellular Na+reduced the sudden increase of myocardial K+ in the first few minutes of reperfusion, and inhibited its decline in the later course of reperfusion. Ischaemia induced a moderate accumulation of myocardial Ca2+ only, but there was a steep increase from the 5th min of reperfusion, and low extracellular Na+also prevented this increase.The results obtained described time dependent changes in myocardial ion contents in the course of reperfusion and indicate the beneficial effect of low extracellular Na+ against reperfusion arrhythmias.

AB - Isolated Guinea pig hearts subjected to global ischaemia were used to investigate whether low extracellular Na+ exerts an anti-arrhythmic action against reperfusion arrhythmias, and the effects of extracellular Na+ manipulation upon myocardial ion contents (Na+, K+ and Ca2+) during ischaemia and reperfusion were studied. Using an optimal concentration of 144 mmol·litre-1 of extracellular Na+, hearts were subjected to 10, 20, 25, 30 or 40 min of global ischaemia followed by 25 min reperfusion. A bell shaped curve was obtained such that with increasing durations of ischaemia from 20 to 30 min there was an increasing incidence of reperfusion arrhythmias. Beyond this optimum (at which 100% exhibited reperfusion induced ventricular fibrillation and tachycardia) there was a decline in the susceptibility of the hearts to arrhythmias. Low extracellular Na+ was given 5 min prior to the global ischaemia and maintained during reperfusion. With extracellular Na+ of 24, 54, 84 and 114 mmol·litre-1, reperfusion induced ventricular fibrillation and tachycardia were reduced from their control incidence of 91% and 100% to 8% (p<0.001) and 17% (p<0.001), 17% (p<0.01) and 17% (p<0.001), 41% (p<0.05) and 50% (p<0.05), and 91% and 91%, respectively. Both ischaemia induced Na+ gain and K+ loss were inhibited by low extracellular Na+ (24 mmol·litre-1). During reperfusion, myocardial Na+ was further increased in the control group and this value was lower in the low extracellular Na+ group. In control hearts, myocardial K+ was suddenly increased during the first 5 min of reperfusion, then continuously decreased until the end of reperfusion. Low extracellular Na+reduced the sudden increase of myocardial K+ in the first few minutes of reperfusion, and inhibited its decline in the later course of reperfusion. Ischaemia induced a moderate accumulation of myocardial Ca2+ only, but there was a steep increase from the 5th min of reperfusion, and low extracellular Na+also prevented this increase.The results obtained described time dependent changes in myocardial ion contents in the course of reperfusion and indicate the beneficial effect of low extracellular Na+ against reperfusion arrhythmias.

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