Subthreshold vagal stimulation suppresses ventricular arrhythmia and inflammatory response in a canine model of acute cardiac ischaemia and reperfusion.

Subthreshold vagal stimulation (SVS) suppresses atrial arrhythmias in canine models and humans. This study was designed to examine whether SVS could decrease ventricular arrhythmia during ischaemia and reperfusion. Twenty-four anaesthetized dogs subjected to 1 h of coronary artery occlusion and 3 h of reperfusion were equally assigned into sham and SVS groups. Subthreshold vagal stimulation was initiated 15 min before coronary occlusion and maintained until the end of the reperfusion period using electrical stimulation on bilateral vagal trunks at 50% below the voltage which slowed the sinus rate. Ventricular arrhythmias were recorded during ischaemia and reperfusion periods. Serum concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), high-mobility group box 1 (HMGB1) and noradrenaline were detected at baseline, at the end of ischaemia and at the end of reperfusion. Area at risk and infarct size were evaluated after 3 h of reperfusion. Compared with the sham group, SVS significantly suppressed ischaemia- and reperfusion-induced ventricular arrhythmias and decreased serum concentrations of CRP, IL-6, TNF-α, HMGB1 and noradrenaline during both the ischaemia period and the reperfusion period. However, SVS did not affect the area at risk, infarct size or the ratio of infarct size to area at risk. This study demonstrated that SVS exerted antiarrhythmic and anti-inflammatory effects in a canine model of ischaemia and reperfusion.