Author + information
- Krekwit Shinlapawittayatorna,b,
- Watthana Nuntaphuma,b,
- Pongpan Tanajaka,b,
- Savitree Thummasorna,b,
- Juthamas Khamseekaewa,b,
- Suwakon Wongjaikama,b,
- Siriporn Chattipakorna,b and
- Nipon Chattipakorna,b
Background: Vagus nerve stimulation (VNS) has been shown to exert cardioprotection against cardiac ischemia/reperfusion (I/R) injury. However, whether the benefit of VNS is mainly due to direct activation of ipsilateral vagal fibers or indirect activation of the contralateral vagal trunk remains unknown. We hypothesized that cardioprotection of VNS requires both ipsilateral and contralateral vagal activity to exert its full benefit.
Methods: Pigs (30-35 kg, n=30) were randomized into 5 groups: I/R, left cervical VNS applied at the ischemic onset (VNS), VNS+left vagus nerve transection (LtVNX), VNS+right vagus nerve transection (RtVNX), and atropine injected 15 min before VNS (I/R+atropine). VNS (3.5 mA, 20 Hz, 21-s ON, 30-s OFF) was initiated at the ischemic onset, and continued until the end of reperfusion. Ischemia was induced by 60-min left anterior descending (LAD) coronary artery occlusion, followed by 120-min reperfusion.
Results: VNS (both intact and LtVNX) significantly decreased the infarct size, arrhythmia score and attenuated cardiac mitochondrial dysfunction (panel A-C, respectively). However, RtVNX had larger infarct size than both VNS treated groups, suggesting a significant influence of contralateral vagal activity on cardioprotection. These beneficial effects of VNS were completely abolished, but not aggravated, by atropine.
Conclusions: VNS requires both ipsilateral and contralateral efferent vagal activity to fully provide its cardioprotection against I/R injury.
Poster Hall, Hall C
Friday, March 17, 2017, 10:00 a.m.-10:45 a.m.
Session Title: Updates in Stable Ischemic Heart Disease
Abstract Category: 3. Acute and Stable Ischemic Heart Disease: Therapy
Presentation Number: 1125-310
- 2017 American College of Cardiology Foundation