Anti-arrhythmic effect of acupuncture pretreatment in the rats subjected to simulative global ischemia and reperfusion—involvement of intracellular Ca(2+) and connexin 43

BACKGROUND: The previous study showed that the cardiac arrhythmias induced by myocardial ischemia and reperfusion were attenuated by the pretreatment of acupuncture; however, the related mechanism is not understood. The present study was therefore designed to determine whether intracellular Ca(2+) ([Ca(2+)](i)) and connexin 43 (Cx(43)) are involved in the mediation of the anti-arrhythmic effect of electro-acupuncture (EA) pretreatment in the rats subjected to simulative global ischemia and reperfusion (SGIR). METHODS: SGIR was made in the isolated heart by a low flow perfusion followed by a flow restoration. Four groups of animals are involved in the present study, including normal control group, SGIR group, EA group and EA plus 18 beta-glycyrrhetinic acid (EAG) group. For EA pretreatment, bilateral Neiguan acupoints (PC6) of the rats were stimulated for 30 min once a day in 3 consecutive days. Cx(43) antagonist was given to the rats in EAG group 30 minutes before the EA pretreatment. The resting [Ca(2+)](i) concentration, calcium oscillation, the contents of total Cx(43) and non-phosphrylated Cx(43) and arrhythmia score were compared among different groups. RESULTS: In EA group, the arrhythmic score, the resting [Ca(2+)](i) concentration and the number of [Ca(2+)](i) oscillations were all significantly less than those in SGIR group (all P < 0.05), and interestingly, after EA pretreatment, the contents of nonphosphated Cx43 in the EA group were significantly lower than that in SGIR group respectively (P < 0.05). However, when the rats were treated with Cx(43) antagonist prior to the EA pretreatment, the protection effects induced by EA pretreatment were reversed. CONCLUSIONS: The results showed that EA pretreatment could produce anti-arrhythmic effect in the rats subjected to SGIR. The anti-arrhythmic effect of EA pretreatment may be due at least partially to the inhibition of SGIR-induced calcium overload and [Ca(2+)](i) oscillations, reduction of non-phosphorylated Cx(43) and the enhancement of the corresponding phosphorylated Cx(43) in the cardiac cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12906-015-0521-y) contains supplementary material, which is available to authorized users.