Is there a role of inducible nitric oxide synthase activation in the delayed antiarrhythmic effect of sodium nitrite?
This study aimed to examine whether inducible nitric oxide synthase (iNOS) plays a role in the delayed antiarrhythmic effect of sodium nitrite. Twenty-one dogs were infused intravenously with sodium nitrite (0.2 μmol·kg –1 ·min –1 ) for 20 min, either in the absence (n = 12) or in the presence of th...
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Published in | Canadian journal of physiology and pharmacology Vol. 95; no. 4; pp. 447 - 454 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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01.04.2017
Canadian Science Publishing NRC Research Press |
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Abstract | This study aimed to examine whether inducible nitric oxide synthase (iNOS) plays a role in the delayed antiarrhythmic effect of sodium nitrite. Twenty-one dogs were infused intravenously with sodium nitrite (0.2 μmol·kg
–1
·min
–1
) for 20 min, either in the absence (n = 12) or in the presence of the iNOS inhibitor S-(2-aminoethyl)-isothiourea (AEST) (total dose 2.0 mg·kg
–1
i.v., n = 9). Control dogs (n = 12) were given saline. Twenty-four hours later, all of the dogs were subjected to a 25 min period occlusion of the left anterior descending coronary artery followed by rapid reperfusion. Dogs treated with AEST and nitrite received again AEST prior to the occlusion. Compared with the controls, sodium nitrite markedly reduced the number of ectopic beats, the number and incidence of ventricular tachycardia, and the incidence of ventricular fibrillation during occlusion and increased survival (0% versus 50%) from the combined ischaemia and reperfusion insult. Although AEST completely inhibited iNOS activity, the nitrite-induced increase in NO bioavailability during occlusion was not substantially modified. Furthermore, AEST attenuated but did not completely abolish the antiarrhythmic effect of nitrite. The marked delayed antiarrhythmic effect of sodium nitrite is not entirely due to the activation of iNOS; other mechanisms may certainly play a role. |
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AbstractList | This study aimed to examine whether inducible nitric oxide synthase (iNOS) plays a role in the delayed antiarrhythmic effect of sodium nitrite. Twenty-one dogs were infused intravenously with sodium nitrite (0.2 [micro]mol x [kg.sup.-1] x [min.sup.-1]) for 20 min, either in the absence (n = 12) or in the presence of the iNOS inhibitor S-(2-aminoethyl)-isothiourea (AEST) (total dose 2.0 mg x [kg.sup.-1] i.v., n = 9). Control dogs (n = 12) were given saline. Twenty-four hours later, all of the dogs were subjected to a 25 min period occlusion of the left anterior descending coronary artery followed by rapid reperfusion. Dogs treated with AEST and nitrite received again AEST prior to the occlusion. Compared with the controls, sodium nitrite markedly reduced the number of ectopic beats, the number and incidence of ventricular tachycardia, and the incidence of ventricular fibrillation during occlusion and increased survival (0% versus 50%) from the combined ischaemia and reperfusion insult. Although AEST completely inhibited iNOS activity, the nitrite-induced increase in NO bioavailability during occlusion was not substantially modified. Furthermore, AEST attenuated but did not completely abolish the antiarrhythmic effect of nitrite. The marked delayed antiarrhythmic effect of sodium nitrite is not entirely due to the activation of iNOS; other mechanisms may certainly play a role. This study aimed to examine whether inducible nitric oxide synthase (iNOS) plays a role in the delayed antiarrhythmic effect of sodium nitrite. Twenty-one dogs were infused intravenously with sodium nitrite (0.2 μmol·kg –1 ·min –1 ) for 20 min, either in the absence (n = 12) or in the presence of the iNOS inhibitor S-(2-aminoethyl)-isothiourea (AEST) (total dose 2.0 mg·kg –1 i.v., n = 9). Control dogs (n = 12) were given saline. Twenty-four hours later, all of the dogs were subjected to a 25 min period occlusion of the left anterior descending coronary artery followed by rapid reperfusion. Dogs treated with AEST and nitrite received again AEST prior to the occlusion. Compared with the controls, sodium nitrite markedly reduced the number of ectopic beats, the number and incidence of ventricular tachycardia, and the incidence of ventricular fibrillation during occlusion and increased survival (0% versus 50%) from the combined ischaemia and reperfusion insult. Although AEST completely inhibited iNOS activity, the nitrite-induced increase in NO bioavailability during occlusion was not substantially modified. Furthermore, AEST attenuated but did not completely abolish the antiarrhythmic effect of nitrite. The marked delayed antiarrhythmic effect of sodium nitrite is not entirely due to the activation of iNOS; other mechanisms may certainly play a role. This study aimed to examine whether inducible nitric oxide synthase (iNOS) plays a role in the delayed antiarrhythmic effect of sodium nitrite. Twenty-one dogs were infused intravenously with sodium nitrite (0.2 [micro]mol x [kg.sup.-1] x [min.sup.-1]) for 20 min, either in the absence (n = 12) or in the presence of the iNOS inhibitor S-(2-aminoethyl)-isothiourea (AEST) (total dose 2.0 mg x [kg.sup.-1] i.v., n = 9). Control dogs (n = 12) were given saline. Twenty-four hours later, all of the dogs were subjected to a 25 min period occlusion of the left anterior descending coronary artery followed by rapid reperfusion. Dogs treated with AEST and nitrite received again AEST prior to the occlusion. Compared with the controls, sodium nitrite markedly reduced the number of ectopic beats, the number and incidence of ventricular tachycardia, and the incidence of ventricular fibrillation during occlusion and increased survival (0% versus 50%) from the combined ischaemia and reperfusion insult. Although AEST completely inhibited iNOS activity, the nitrite-induced increase in NO bioavailability during occlusion was not substantially modified. Furthermore, AEST attenuated but did not completely abolish the antiarrhythmic effect of nitrite. The marked delayed antiarrhythmic effect of sodium nitrite is not entirely due to the activation of iNOS; other mechanisms may certainly play a role. Key words: arrhythmias, sodium nitrite, delayed protection, ischaemia-reperfusion, nitric oxide. Cette etude portait sur le role eventuel de l'oxyde nitrique synthase inductible (iNOS) dans les effets antiarythmiques retards du nitrite de sodium. Nous avons perfuse par voie intraveineuse du nitrite de sodium (a 0,2 [micro]mol x [kg.sup.-1] x [min.sup.-1]) chez 21 chiens pendant 20 min, en absence (n = 12) ou en presence de S-(2-aminoethyl)-isothio-uree (AEST), un inhibiteur de l'iNOS (dose totale 2,0mg x [kg.sup.-1] i.v., n = 9). Nous avons administre une solution saline aux chiens temoins (n = 12). Vingt-quatre heures plus tard, nous avons procede chez tous les chiens a une ligature de 25 min de l'artere interventriculaire anterieure, suivie d'une reperfusion rapide. Les chiens exposes a l'AEST et au nitrite ont de nouveau recu de l'AEST avant l'occlusion. Par rapport au groupe temoin, le nitrite de sodium a entraine une reduction importante du nombre de battements ectopiques, du nombre et du taux d'apparition de tachycardies ventriculaires ainsi que du taux d'apparition de fibrillations ventriculaires pendant l'occlusion. Le produit a aussi permis d'augmenter le taux de survie (0 % versus 50 %) apres les interventions d'ischemie et de reperfusion combinees. Bien que l'AEST n'ait pas entraine d'inhibition complete de l'activite de l'iNOS, l'augmentation de la biodisponibilite du NO provoquee par le nitrite pendant l'occlusion n'etait pas modifiee de facon notable. De plus, l'AEST aentraine une attenuation sans abolition complete des effets antiarythmiques du nitrite. L'effet antiarythmique retard marque du nitrite de sodium n'est pas entierement cause par l'activation de l'iNOS; d'autres modes d'action pourraient certainement avoir un role a jouer. [Traduit par la Redaction] Mots-cles : arythmies, nitrite de sodium, protection retard, ischemie-reperfusion, oxyde nitrique. This study aimed to examine whether inducible nitric oxide synthase (iNOS) plays a role in the delayed antiarrhythmic effect of sodium nitrite. Twenty-one dogs were infused intravenously with sodium nitrite (0.2 μmol·kg ·min ) for 20 min, either in the absence (n = 12) or in the presence of the iNOS inhibitor S-(2-aminoethyl)-isothiourea (AEST) (total dose 2.0 mg·kg i.v., n = 9). Control dogs (n = 12) were given saline. Twenty-four hours later, all of the dogs were subjected to a 25 min period occlusion of the left anterior descending coronary artery followed by rapid reperfusion. Dogs treated with AEST and nitrite received again AEST prior to the occlusion. Compared with the controls, sodium nitrite markedly reduced the number of ectopic beats, the number and incidence of ventricular tachycardia, and the incidence of ventricular fibrillation during occlusion and increased survival (0% versus 50%) from the combined ischaemia and reperfusion insult. Although AEST completely inhibited iNOS activity, the nitrite-induced increase in NO bioavailability during occlusion was not substantially modified. Furthermore, AEST attenuated but did not completely abolish the antiarrhythmic effect of nitrite. The marked delayed antiarrhythmic effect of sodium nitrite is not entirely due to the activation of iNOS; other mechanisms may certainly play a role. This study aimed to examine whether inducible nitric oxide synthase (iNOS) plays a role in the delayed antiarrhythmic effect of sodium nitrite. Twenty-one dogs were infused intravenously with sodium nitrite (0.2 μmol·kg-1·min-1) for 20 min, either in the absence (n = 12) or in the presence of the iNOS inhibitor S-(2-aminoethyl)-isothiourea (AEST) (total dose 2.0 mg·kg-1 i.v., n = 9). Control dogs (n = 12) were given saline. Twenty-four hours later, all of the dogs were subjected to a 25 min period occlusion of the left anterior descending coronary artery followed by rapid reperfusion. Dogs treated with AEST and nitrite received again AEST prior to the occlusion. Compared with the controls, sodium nitrite markedly reduced the number of ectopic beats, the number and incidence of ventricular tachycardia, and the incidence of ventricular fibrillation during occlusion and increased survival (0% versus 50%) from the combined ischaemia and reperfusion insult. Although AEST completely inhibited iNOS activity, the nitrite-induced increase in NO bioavailability during occlusion was not substantially modified. Furthermore, AEST attenuated but did not completely abolish the antiarrhythmic effect of nitrite. The marked delayed antiarrhythmic effect of sodium nitrite is not entirely due to the activation of iNOS; other mechanisms may certainly play a role. |
Abstract_FL | Cette étude portait sur le rôle éventuel de l’oxyde nitrique synthase inductible (iNOS) dans les effets antiarythmiques retards du nitrite de sodium. Nous avons perfusé par voie intraveineuse du nitrite de sodium (à 0,2 μmol·kg
–1
·min
–1
) chez 21 chiens pendant 20 min, en absence (n = 12) ou en présence de S-(2-aminoéthyl)-isothio-urée (AEST), un inhibiteur de l’iNOS (dose totale 2,0 mg·kg
–1
i.v., n = 9). Nous avons administré une solution saline aux chiens témoins (n = 12). Vingt-quatre heures plus tard, nous avons procédé chez tous les chiens à une ligature de 25 min de l’artère interventriculaire antérieure, suivie d’une reperfusion rapide. Les chiens exposés à l’AEST et au nitrite ont de nouveau reçu de l’AEST avant l’occlusion. Par rapport au groupe témoin, le nitrite de sodium a entraîné une réduction importante du nombre de battements ectopiques, du nombre et du taux d’apparition de tachycardies ventriculaires ainsi que du taux d’apparition de fibrillations ventriculaires pendant l’occlusion. Le produit a aussi permis d’augmenter le taux de survie (0 % versus 50 %) après les interventions d’ischémie et de reperfusion combinées. Bien que l’AEST n’ait pas entraîné d’inhibition complète de l’activité de l’iNOS, l’augmentation de la biodisponibilité du NO provoquée par le nitrite pendant l’occlusion n’était pas modifiée de façon notable. De plus, l’AEST a entraîné une atténuation sans abolition complète des effets antiarythmiques du nitrite. L’effet antiarythmique retard marqué du nitrite de sodium n’est pas entièrement causé par l’activation de l’iNOS; d’autres modes d’action pourraient certainement avoir un rôle à jouer. [Traduit par la Rédaction] |
Audience | Academic |
Author | Végh, Ágnes Demeter-Haludka, Vivien Juhász, László Kovác, Mária Gardi, János |
Author_xml | – sequence: 1 givenname: Vivien surname: Demeter-Haludka fullname: Demeter-Haludka, Vivien organization: Department of Pharmacology and Pharmacotherapy, University of Szeged, Albert-Szent Györgyi Medical Centre, Szeged H-6720, Hungary – sequence: 2 givenname: László surname: Juhász fullname: Juhász, László organization: Department of Pharmacology and Pharmacotherapy, University of Szeged, Albert-Szent Györgyi Medical Centre, Szeged H-6720, Hungary – sequence: 3 givenname: Mária surname: Kovác fullname: Kovác, Mária organization: Department of Pharmacology and Pharmacotherapy, University of Szeged, Albert-Szent Györgyi Medical Centre, Szeged H-6720, Hungary – sequence: 4 givenname: János surname: Gardi fullname: Gardi, János organization: First Department of Internal Medicine, University of Szeged, Albert-Szent Györgyi Medical Centre, Szeged H-6720, Hungary – sequence: 5 givenname: Ágnes surname: Végh fullname: Végh, Ágnes organization: Department of Pharmacology and Pharmacotherapy, University of Szeged, Albert-Szent Györgyi Medical Centre, Szeged H-6720, Hungary |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28177694$$D View this record in MEDLINE/PubMed |
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Keywords | nitrite de sodium arythmies nitric oxide oxyde nitrique arrhythmias ischaemia–reperfusion ischémie–reperfusion sodium nitrite delayed protection protection retard |
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SubjectTerms | Animals Anti-Arrhythmia Agents - administration & dosage Anti-Arrhythmia Agents - pharmacology Anti-Arrhythmia Agents - therapeutic use Arrhythmia arrhythmias Arrhythmias, Cardiac - etiology Arrhythmias, Cardiac - prevention & control arythmies beta-Aminoethyl Isothiourea - pharmacology Coronary vessels delayed protection Dogs Health aspects Hemodynamics - drug effects ischaemia–reperfusion Ischemia Ischemic Preconditioning, Myocardial - methods ischémie–reperfusion Myocardial Reperfusion Injury - complications Myocardial Reperfusion Injury - etiology Nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type II - antagonists & inhibitors Nitric Oxide Synthase Type II - metabolism nitrite de sodium oxyde nitrique protection retard Sodium nitrite Sodium Nitrite - administration & dosage Sodium Nitrite - pharmacology Sodium Nitrite - therapeutic use Studies Tachycardia, Ventricular - etiology Tachycardia, Ventricular - prevention & control |
Title | Is there a role of inducible nitric oxide synthase activation in the delayed antiarrhythmic effect of sodium nitrite? |
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