Anti-arrhythmic effects of atrial ganglionated plexi stimulation is accompanied by preservation of connexin43 protein in ischemia-reperfusion canine model.

BACKGROUND Vagal nerve stimulation (VNS) has been shown to provide a protective effect against ischemia/reperfusion (I/R)-related arrhythmias by preventing the loss of Connexin43 (Cx43). Our previous studies showed that atrial epicardial ganglionated plexus stimulation (GPS) might exert a VNS-like effect on ventricular electrophysiology. OBJECTIVES To investigate whether GPS could preserve Cx43 and reduce I/R induced ventricular arrhythmia. METHODS Sixteen dogs were randomly divided into GPS group (N = 8, receiving GPS) and Sham group (N = 8, receiving sham GPS). Ventricular effective refractory period (ERP) and heart rate variability (HRV) were measured at baseline and 1 h after GPS. Myocardial I/R was then performed. Ventricular arrhythmia occurred during the first hour after reperfusion was measured and myocardial tissue from the peri-infarct zone was excised for immunohistological analysis. In another 4 dogs (Control group, receiving sham GPS and sham I/R), myocardial tissue from the corresponding area was also excised. RESULTS Compared with the Sham group, GPS caused a significant increase in ventricular ERP and HRV, and a significant decrease in I/R-induced ventricular arrhythmias. Western blotting revealed a marked reduction in the amount of phosphorylated Cx43 and total Cx43 in the Sham group, whereas no significant change was observed in the GPS group compared with the Control group. Immunohistochemistry results confirmed that the myocardial I/R-induced loss of phosphorylated Cx43 from the intercellular junctions was prevented by GPS. CONCLUSION GPS protects against I/R induced ventricular arrhythmias, accompanied by preserving Cx43.