Eicosapentaenoic acid reduces the pulmonary vein arrhythmias through nitric oxide

Kazuyoshi Suenari, Yao Chang Chen, Yu Hsun Kao, Chen Chuan Cheng, Yung Kuo Lin, Yasuki Kihara, Yi Jen Chen, Shih Ann Chen

研究成果: 雜誌貢獻文章

16 引文 (Scopus)

摘要

Aims: Omega-3 polyunsaturated fatty acids can modulate cardiac electrophysiology and reduce the genesis of atrial fibrillation. This study investigates the potential mechanisms through which eicosapentaenoic acid (EPA) reduces pulmonary vein (PV) arrhythmogenesis. Main methods: Conventional microelectrodes were used to record the action potentials (APs), before and after the EPA (0.1 μM and 1.0 μM) administration with and without the presence of a nitric oxide (NO) synthase inhibitor (L-NAME, 100 μM) in isolated rabbit PV tissue preparations. Furthermore, indo-1 fluorimetric ratio technique was used to evaluate intracellular calcium in isolated single PV cardiomyocytes with or without incubation of EPA (1.0 μM, 30 min). Key findings: EPA concentration-dependently reduced the PV spontaneous beating rate (P <0.05). EPA (1.0 μM) also reduced the amplitude of delayed afterdepolarizations (P <0.05). EPA hyperpolarized the maximal diastolic potential (MDP), shortened AP duration, increased AP amplitude (APA), and reduced diastolic tension and contractility. However, EPA in the presence of L-NAME or omega-9 fatty acids (oleic acid, 1.0 μM) did not have any effect on PV spontaneous activity, AP morphology, or contractile force. A linear regression shows that the decrease in PV spontaneous beating rates induced by EPA correlated well with the changes of MDP, APA, diastolic tension, and contractile force of PVs. In addition, intracellular Ca2+ transient and sarcoplasmic reticulum Ca2+ content were significantly more decreased in the EPA-treated cardiomyocytes than in control PV cardiomyocytes as observed by indo-1 fluorescence. Significance: EPA reduces PV arrhythmogenesis through the mechanoelectrical feedback generated by NO production.

原文英語
頁(從 - 到)129-136
頁數8
期刊Life Sciences
89
發行號3-4
DOIs
出版狀態已發佈 - 七月 18 2011

指紋

Eicosapentaenoic Acid
Pulmonary Veins
Cardiac Arrhythmias
Nitric Oxide
Action Potentials
Cardiac Myocytes
NG-Nitroarginine Methyl Ester
Cardiac Electrophysiology
Microelectrodes
Omega-3 Fatty Acids
Sarcoplasmic Reticulum
Oleic Acid
Unsaturated Fatty Acids
Linear regression
Nitric Oxide Synthase
Atrial Fibrillation
Linear Models
Fatty Acids
Fluorescence
Tissue

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Biochemistry, Genetics and Molecular Biology(all)

引用此文

Eicosapentaenoic acid reduces the pulmonary vein arrhythmias through nitric oxide. / Suenari, Kazuyoshi; Chen, Yao Chang; Kao, Yu Hsun; Cheng, Chen Chuan; Lin, Yung Kuo; Kihara, Yasuki; Chen, Yi Jen; Chen, Shih Ann.

於: Life Sciences, 卷 89, 編號 3-4, 18.07.2011, p. 129-136.

研究成果: 雜誌貢獻文章

Suenari, Kazuyoshi ; Chen, Yao Chang ; Kao, Yu Hsun ; Cheng, Chen Chuan ; Lin, Yung Kuo ; Kihara, Yasuki ; Chen, Yi Jen ; Chen, Shih Ann. / Eicosapentaenoic acid reduces the pulmonary vein arrhythmias through nitric oxide. 於: Life Sciences. 2011 ; 卷 89, 編號 3-4. 頁 129-136.
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abstract = "Aims: Omega-3 polyunsaturated fatty acids can modulate cardiac electrophysiology and reduce the genesis of atrial fibrillation. This study investigates the potential mechanisms through which eicosapentaenoic acid (EPA) reduces pulmonary vein (PV) arrhythmogenesis. Main methods: Conventional microelectrodes were used to record the action potentials (APs), before and after the EPA (0.1 μM and 1.0 μM) administration with and without the presence of a nitric oxide (NO) synthase inhibitor (L-NAME, 100 μM) in isolated rabbit PV tissue preparations. Furthermore, indo-1 fluorimetric ratio technique was used to evaluate intracellular calcium in isolated single PV cardiomyocytes with or without incubation of EPA (1.0 μM, 30 min). Key findings: EPA concentration-dependently reduced the PV spontaneous beating rate (P <0.05). EPA (1.0 μM) also reduced the amplitude of delayed afterdepolarizations (P <0.05). EPA hyperpolarized the maximal diastolic potential (MDP), shortened AP duration, increased AP amplitude (APA), and reduced diastolic tension and contractility. However, EPA in the presence of L-NAME or omega-9 fatty acids (oleic acid, 1.0 μM) did not have any effect on PV spontaneous activity, AP morphology, or contractile force. A linear regression shows that the decrease in PV spontaneous beating rates induced by EPA correlated well with the changes of MDP, APA, diastolic tension, and contractile force of PVs. In addition, intracellular Ca2+ transient and sarcoplasmic reticulum Ca2+ content were significantly more decreased in the EPA-treated cardiomyocytes than in control PV cardiomyocytes as observed by indo-1 fluorescence. Significance: EPA reduces PV arrhythmogenesis through the mechanoelectrical feedback generated by NO production.",
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T1 - Eicosapentaenoic acid reduces the pulmonary vein arrhythmias through nitric oxide

AU - Suenari, Kazuyoshi

AU - Chen, Yao Chang

AU - Kao, Yu Hsun

AU - Cheng, Chen Chuan

AU - Lin, Yung Kuo

AU - Kihara, Yasuki

AU - Chen, Yi Jen

AU - Chen, Shih Ann

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N2 - Aims: Omega-3 polyunsaturated fatty acids can modulate cardiac electrophysiology and reduce the genesis of atrial fibrillation. This study investigates the potential mechanisms through which eicosapentaenoic acid (EPA) reduces pulmonary vein (PV) arrhythmogenesis. Main methods: Conventional microelectrodes were used to record the action potentials (APs), before and after the EPA (0.1 μM and 1.0 μM) administration with and without the presence of a nitric oxide (NO) synthase inhibitor (L-NAME, 100 μM) in isolated rabbit PV tissue preparations. Furthermore, indo-1 fluorimetric ratio technique was used to evaluate intracellular calcium in isolated single PV cardiomyocytes with or without incubation of EPA (1.0 μM, 30 min). Key findings: EPA concentration-dependently reduced the PV spontaneous beating rate (P <0.05). EPA (1.0 μM) also reduced the amplitude of delayed afterdepolarizations (P <0.05). EPA hyperpolarized the maximal diastolic potential (MDP), shortened AP duration, increased AP amplitude (APA), and reduced diastolic tension and contractility. However, EPA in the presence of L-NAME or omega-9 fatty acids (oleic acid, 1.0 μM) did not have any effect on PV spontaneous activity, AP morphology, or contractile force. A linear regression shows that the decrease in PV spontaneous beating rates induced by EPA correlated well with the changes of MDP, APA, diastolic tension, and contractile force of PVs. In addition, intracellular Ca2+ transient and sarcoplasmic reticulum Ca2+ content were significantly more decreased in the EPA-treated cardiomyocytes than in control PV cardiomyocytes as observed by indo-1 fluorescence. Significance: EPA reduces PV arrhythmogenesis through the mechanoelectrical feedback generated by NO production.

AB - Aims: Omega-3 polyunsaturated fatty acids can modulate cardiac electrophysiology and reduce the genesis of atrial fibrillation. This study investigates the potential mechanisms through which eicosapentaenoic acid (EPA) reduces pulmonary vein (PV) arrhythmogenesis. Main methods: Conventional microelectrodes were used to record the action potentials (APs), before and after the EPA (0.1 μM and 1.0 μM) administration with and without the presence of a nitric oxide (NO) synthase inhibitor (L-NAME, 100 μM) in isolated rabbit PV tissue preparations. Furthermore, indo-1 fluorimetric ratio technique was used to evaluate intracellular calcium in isolated single PV cardiomyocytes with or without incubation of EPA (1.0 μM, 30 min). Key findings: EPA concentration-dependently reduced the PV spontaneous beating rate (P <0.05). EPA (1.0 μM) also reduced the amplitude of delayed afterdepolarizations (P <0.05). EPA hyperpolarized the maximal diastolic potential (MDP), shortened AP duration, increased AP amplitude (APA), and reduced diastolic tension and contractility. However, EPA in the presence of L-NAME or omega-9 fatty acids (oleic acid, 1.0 μM) did not have any effect on PV spontaneous activity, AP morphology, or contractile force. A linear regression shows that the decrease in PV spontaneous beating rates induced by EPA correlated well with the changes of MDP, APA, diastolic tension, and contractile force of PVs. In addition, intracellular Ca2+ transient and sarcoplasmic reticulum Ca2+ content were significantly more decreased in the EPA-treated cardiomyocytes than in control PV cardiomyocytes as observed by indo-1 fluorescence. Significance: EPA reduces PV arrhythmogenesis through the mechanoelectrical feedback generated by NO production.

KW - Atrial fibrillation

KW - Electrophysiology

KW - Fatty acids

KW - Nitric oxide

KW - Pulmonary vein

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