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This Article Full Text Full Text (PDF) All Versions of this Article: 93/8/931    most recent expphysiol.2007.041558v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by del Rio, C. L. Articles by Billman, G. E. PubMed PubMed Citation Articles by del Rio, C. L. Articles by Billman, G. E. Related Collections Cardiovascular control

Departments of ¹ Physiology & Cell Biology² Electrical & Computer Engineering⁴ Biomedical Engineering⁵ Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA ³ Burdon Sanderson Cardiac Science Centre, Departments of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK

Parasympathetic activity during acute coronary artery occlusion (CAO) can protect against ischaemia-induced malignant arrhythmias; nonetheless, the mechanism mediating this protection remains unclear. During CAO, myocardial electrotonic uncoupling is associated with autonomically mediated immediate (i.e. type 1A) arrhythmias and can modulate pro-arrhythmic dispersion of repolarization. Therefore, 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. Anaesthetized dogs were instrumented for MEI measurements, and left circumflex coronary arterial occlusions were performed in intact (CTRL) and vagotomized (VAG) animals. The CAO was followed by either vagotomy (CTRL) or vagal nerve stimulation (VNS, 10 Hz, 10 V) in the VAG dogs. Vagal nerve stimulation was studied in two additional sets of animals. In one set heart rate (HR) was maintained by pacing (220 beats min^–1), while in the other set bilateral stellectomy preceded CAO. The 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 with intact control dogs (+43 ± 5 , from 620 ± 20 , n = 7). Acute vagotomy during ischaemia abruptly increased HR (from 155 ± 11 to 193 ± 15 beats min^–1) and MEI (+12 ± 1.1 , from 663 ± 18 ). In contrast, VNS during ischaemia (n = 11) abruptly reduced HR (from 206 ± 6 to 73 ± 9 beats min^–1) and MEI (–16 ± 2 , from 700 ± 44 ). These effects of VNS were eliminated by pacing but not by bilateral stellectomy. Vagal nerve stimulation during CAO also attenuated ECG-derived indices of ischaemia (e.g. ST segment, 0.22 ± 0.03 versus 0.15 ± 0.03 mV) and of rate-corrected repolarization dispersion [terminal portion of T wave (TPEc), 84.5 ± 4.2 versus 65.8 ± 5.9 ms; QTc, 340 ± 8 versus 254 ± 16 ms]. Vagal nerve stimulation during myocardial ischaemia exerts negative chronotropic effects, limiting early ischaemic electrotonic uncoupling and dispersion of repolarization, possibly via a decreased myocardial metabolic demand.

(Received 26 November 2007; accepted after revision 27 March 2008; first published online 30 March 2008)
Corresponding author G. E. Billman: Department of Physiology and Cell Biology, The Ohio State University, 1645 Neil Avenue, 305 Hamilton Hall, Columbus, OH 43210, USA. Email: billman.1{at}osu.edu