2017
DOI: 10.1177/1179546817739523
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Calcium Dynamics and Cardiac Arrhythmia

Abstract: This Special Collection will gather all studies highlighting recent advances in theoretical and experimental studies of arrhythmia, with a specific focus on research seeking to elucidate links between calcium homeostasis in cardiac cells and organ-scale disruption of heart rhythm.

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Cited by 12 publications
(9 citation statements)
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References 38 publications
(19 reference statements)
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“…Calcium ions play an essential role not only in myocardial contraction but also in the occurrence of arrhythmia. 32 , 33 Acidemia increases extracellular H + level and then promotes the exchange between the extracellular H + and intracellular Ca 2+ , decreasing the intracellular Ca 2+ levels and reduces the contractility of the heart muscle, finally leads to hypoinfusion of vital organs. Besides, H + -Ca 2+ exchange promotes Ca 2+ translates into cell, shortening the second stages and the whole action potential, finally increases the risk of arrhythmia.…”
Section: Discussionmentioning
confidence: 99%
“…Calcium ions play an essential role not only in myocardial contraction but also in the occurrence of arrhythmia. 32 , 33 Acidemia increases extracellular H + level and then promotes the exchange between the extracellular H + and intracellular Ca 2+ , decreasing the intracellular Ca 2+ levels and reduces the contractility of the heart muscle, finally leads to hypoinfusion of vital organs. Besides, H + -Ca 2+ exchange promotes Ca 2+ translates into cell, shortening the second stages and the whole action potential, finally increases the risk of arrhythmia.…”
Section: Discussionmentioning
confidence: 99%
“…The tube formation of HUVEC cells was facilitated by exosomes from nonirradiated hp-MSCs, but not the irradiated hp-MSCs. The homeostasis of calcium transient is a crucial factor for maintaining normal cardiac rhythm (27). Following ischemia/reperfusion injury, the internal levels of calcium in H9c2 cells increased in a time-dependent manner (28), and calcium overload in H9c2 cells may further accelerate reperfusion injury (29).…”
Section: Discussionmentioning
confidence: 99%
“…Early afterdepolarizations are a consequence of untimely LTCC reopening and delayed afterdepolarizations occur because of Ca 2+ leaks from the sarcoplasmic reticulum and subsequent substitution of 1 Ca 2+ ion for 3 Na + ions by the NCX. 34,[47][48][49] The major role of Ca 2+ ions in the processes of myocardial contraction and relaxation suggests that a reasonable use of Ca 2+ salts to increase the concentration of these ions on both sides of sarcolemma may cause positive inotropic and chronotropic effects. Indeed, it is a common practice among cardiac anesthesiologists to administer CaCl 2 during weaning from CPB in order to improve cardiac contractility.…”
Section: Ca 2+ Homeostasis and Role In Excitation-contraction Couplinmentioning
confidence: 99%