Vagus nerve stimulation initiated late during ischemia, but not reperfusion, exerts cardioprotection via amelioration of cardiac mitochondrial dysfunction
© 2014 Heart Rhythm Society. All rights reserved. Objective This study aimed to determine whether VNS applied during ischemia or at the onset of reperfusion exerts differential cardioprotection against cardiac I/R injury. Methods Twenty-eight swine (25-30 kg) were randomized into 4 groups: Control (...
Saved in:
Main Authors: | , , , , , , , , |
---|---|
Format: | Article |
Published: |
Elsevier
2015
|
Subjects: | |
Online Access: | http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84919383950&origin=inward http://cmuir.cmu.ac.th/handle/6653943832/38009 |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Institution: | Chiang Mai University |
id |
th-cmuir.6653943832-38009 |
---|---|
record_format |
dspace |
spelling |
th-cmuir.6653943832-380092015-06-16T03:59:36Z Vagus nerve stimulation initiated late during ischemia, but not reperfusion, exerts cardioprotection via amelioration of cardiac mitochondrial dysfunction Shinlapawittayatorn,K. Chinda,K. Palee,S. Surinkaew,S. Kumfu,S. Kumphune,S. Chattipakorn,S.C. KenKnight,B.H. Chattipakorn,N. Cardiology and Cardiovascular Medicine Physiology (medical) © 2014 Heart Rhythm Society. All rights reserved. Objective This study aimed to determine whether VNS applied during ischemia or at the onset of reperfusion exerts differential cardioprotection against cardiac I/R injury. Methods Twenty-eight swine (25-30 kg) were randomized into 4 groups: Control (sham-operated, no VNS), VNS-ischemia (VNS applied during ischemia), VNS-reperfusion (VNS applied during reperfusion), and VNS-ischemia+atropine (VNS applied during ischemia with 1 mg/kg atropine administration). Ischemia was induced by left anterior descending (LAD) coronary artery occlusion for 60 minutes, followed by 120 minutes of reperfusion. VNS was applied either 30 minutes after LAD coronary artery occlusion or at the onset of reperfusion and continued until the end of reperfusion. Cardiac function, infarct size, myocardial levels of connexin 43, cytochrome c, tumor necrosis factor α, and interleukin 4, and cardiac mitochondrial function were determined. Results VNS applied 30 minutes after LAD coronary artery occlusion, but not at reperfusion, markedly reduced ventricular fibrillation incidence and infarct size (~59%), improved cardiac function; attenuated cardiac mitochondrial reactive oxygen species production, depolarization, swelling, and cytochrome c release; and increased the amount of phosphorylated connexin 43 and interleukin 4 as compared with the Control group. These beneficial effects of VNS were abolished by atropine. Conclusion VNS could provide significant cardioprotective effects even when initiated later during ischemia, but was not effective after reperfusion. These findings indicate the importance of timing of VNS initiation and warrant the potential clinical application of VNS in protecting myocardium at risk of I/R injury. Background We previously reported that vagus nerve stimulation (VNS) applied immediately at the onset of cardiac ischemia provides cardioprotection against cardiac ischemic-reperfusion (I/R) injury. 2015-06-16T03:59:35Z 2015-06-16T03:59:35Z 2014-01-01 Article 15475271 2-s2.0-84919383950 10.1016/j.hrthm.2014.08.001 http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84919383950&origin=inward http://cmuir.cmu.ac.th/handle/6653943832/38009 Elsevier |
institution |
Chiang Mai University |
building |
Chiang Mai University Library |
country |
Thailand |
collection |
CMU Intellectual Repository |
topic |
Cardiology and Cardiovascular Medicine Physiology (medical) |
spellingShingle |
Cardiology and Cardiovascular Medicine Physiology (medical) Shinlapawittayatorn,K. Chinda,K. Palee,S. Surinkaew,S. Kumfu,S. Kumphune,S. Chattipakorn,S.C. KenKnight,B.H. Chattipakorn,N. Vagus nerve stimulation initiated late during ischemia, but not reperfusion, exerts cardioprotection via amelioration of cardiac mitochondrial dysfunction |
description |
© 2014 Heart Rhythm Society. All rights reserved. Objective This study aimed to determine whether VNS applied during ischemia or at the onset of reperfusion exerts differential cardioprotection against cardiac I/R injury. Methods Twenty-eight swine (25-30 kg) were randomized into 4 groups: Control (sham-operated, no VNS), VNS-ischemia (VNS applied during ischemia), VNS-reperfusion (VNS applied during reperfusion), and VNS-ischemia+atropine (VNS applied during ischemia with 1 mg/kg atropine administration). Ischemia was induced by left anterior descending (LAD) coronary artery occlusion for 60 minutes, followed by 120 minutes of reperfusion. VNS was applied either 30 minutes after LAD coronary artery occlusion or at the onset of reperfusion and continued until the end of reperfusion. Cardiac function, infarct size, myocardial levels of connexin 43, cytochrome c, tumor necrosis factor α, and interleukin 4, and cardiac mitochondrial function were determined. Results VNS applied 30 minutes after LAD coronary artery occlusion, but not at reperfusion, markedly reduced ventricular fibrillation incidence and infarct size (~59%), improved cardiac function; attenuated cardiac mitochondrial reactive oxygen species production, depolarization, swelling, and cytochrome c release; and increased the amount of phosphorylated connexin 43 and interleukin 4 as compared with the Control group. These beneficial effects of VNS were abolished by atropine. Conclusion VNS could provide significant cardioprotective effects even when initiated later during ischemia, but was not effective after reperfusion. These findings indicate the importance of timing of VNS initiation and warrant the potential clinical application of VNS in protecting myocardium at risk of I/R injury. Background We previously reported that vagus nerve stimulation (VNS) applied immediately at the onset of cardiac ischemia provides cardioprotection against cardiac ischemic-reperfusion (I/R) injury. |
format |
Article |
author |
Shinlapawittayatorn,K. Chinda,K. Palee,S. Surinkaew,S. Kumfu,S. Kumphune,S. Chattipakorn,S.C. KenKnight,B.H. Chattipakorn,N. |
author_facet |
Shinlapawittayatorn,K. Chinda,K. Palee,S. Surinkaew,S. Kumfu,S. Kumphune,S. Chattipakorn,S.C. KenKnight,B.H. Chattipakorn,N. |
author_sort |
Shinlapawittayatorn,K. |
title |
Vagus nerve stimulation initiated late during ischemia, but not reperfusion, exerts cardioprotection via amelioration of cardiac mitochondrial dysfunction |
title_short |
Vagus nerve stimulation initiated late during ischemia, but not reperfusion, exerts cardioprotection via amelioration of cardiac mitochondrial dysfunction |
title_full |
Vagus nerve stimulation initiated late during ischemia, but not reperfusion, exerts cardioprotection via amelioration of cardiac mitochondrial dysfunction |
title_fullStr |
Vagus nerve stimulation initiated late during ischemia, but not reperfusion, exerts cardioprotection via amelioration of cardiac mitochondrial dysfunction |
title_full_unstemmed |
Vagus nerve stimulation initiated late during ischemia, but not reperfusion, exerts cardioprotection via amelioration of cardiac mitochondrial dysfunction |
title_sort |
vagus nerve stimulation initiated late during ischemia, but not reperfusion, exerts cardioprotection via amelioration of cardiac mitochondrial dysfunction |
publisher |
Elsevier |
publishDate |
2015 |
url |
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84919383950&origin=inward http://cmuir.cmu.ac.th/handle/6653943832/38009 |
_version_ |
1681421395151552512 |