Received November 26, 2007
Revised January 9, 2008
Accepted after revision March 27, 2008
Cardiovascular Control [210]
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Acute Vagal Nerve Stimulation Attenuates Early Passive Electrical Changes Induced by Myocardial Ischemia: Heart Rate Mediated Attenuation
Carlos L del Rio 1,
Tom A Dawson 2,
Bradley D Clymer 1,
David J Paterson 3,
George E Billman 1*
1 The Ohio State University
2 Oxford University
3 University of Oxford
* To whom correspondence should be addressed. E-mail: billman.1{at}osu.edu.
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Abstract |
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Parasympathetic activity during acute coronary artery occlusion (CAO) can protect against ischemia-induced malignant arrhythmias; nonetheless, the mechanism mediating this protection remains unclear. During CAO, myocardial electrotonic uncoupling is associated with autonomically mediated 1A-arrhythmias and can modulate pro-arrhythmic dispersion of repolarization. Thus, the effects of acutely enhanced or decreased cardiac parasympathetic activity on early electrotonic coupling during CAO, as measured by myocardial electrical impedance (MEI), were investigated. Anesthetized dogs were instrumented for MEI measurements, and left-circumflex occlusions were performed in intact (CTRL) and vagotomized (VAG) animals. CAO was followed by either vagotomy (CTRL) or vagal nerve stimulation (VNS, 10 Hz, 10V) in the VAG dogs. VNS was studied in two additional sets of animals. In one set heart rate (HR) was maintained by pacing (220 bpm), while in the other set bilateral stellectomy preceded CAO. MEI increased after CAO in all animals. A larger MEI increase was observed in vagotomized animals (+85 ± 9
from 611 ± 24, n = 16) when compared to intact controls (+43 ± 5 from 620 ± 20, n = 7). Acute vagotomy during ischemia abruptly increased HR (from 155 ± 11 bpm to 193 ± 15 bpm) and MEI (+12 ± 1.1, from 663 ± 18). In contrast, VNS during ischemia (n = 11) abruptly reduced HR (from 206 ± 6 to 73 ± 9 bpm) and MEI (-16 ± 2, from 700 ± 44). These effects of VNS were eliminated by pacing but not by bilateral stellectomy. VNS during CAO also attenuated ECG-derived indices of ischemia (e.g., ST-segment: 0.22 ± 0.03 vs. 0.15 ± 0.03 mV) and of rate-corrected repolarization dispersion (TPEc: 84.5 ± 4.2 vs. 65.8 ± 5.9 ms, QTc: 340 ± 8 vs. 254 ± 16 ms). VNS during myocardial ischemia exerts negative chronotropic effects, limiting early ischemic electrotonic uncoupling and dispersion of repolarization, possibly via a decreased myocardial metabolic demand.
Key Words:
Cardiac arrhythmia, Ischaemia, Vagus
