Antiarrhythmic Effect of Acupuncture Pretreatment in Rats Subjected to Simulative Global Ischemia and Reperfusion — Involvement of Adenylate Cyclase, Protein Kinase A, and L-Type Ca2+ Channel

Abstract

Our previous study showed that electro-acupuncture (EA) pretreatment protects the heart from injury of ischemia. The present study explored further whether adenylate cyclase (AC), protein kinase A (PKA), and L-type Ca(2+) channel, the beta(1)-AR signaling components modulating intracellular Ca(2+) ([Ca(2+)](i)), are involved in the mediation of the antiarrhythmic effect of EA pretreatment in the rats from which the hearts were subsequently isolated and subjected to simulative global ischemia and reperfusion (SGIR). SGIR was performed by perfusing the isolated heart at a low flow followed by normal perfusion. Adult rats were randomized into four groups, namely, normal control (NC), SGIR, EA, and NC plus EA (NCEA) groups. The rats in the EA and NCEA groups were given EA pretreatment at bilateral Neiguan points (PC6) for 30 min once a day in 3 consecutive days before the hearts were isolated and perfused. The arrhythmia score and the response of [Ca(2+)](i) to the activators of AC, PKA, and L-type Ca(2+) channel in single ventricular myocyte isolated from the hearts subjected to SGIR were compared among the groups. The results showed that the arrhythmia score was significantly higher in the SGIR group as compared with the NC and NCEA groups. The SGIR-enhanced arrhythmia score was significantly attenuated in the EA group. More interesting, EA pretreatment also attenuated the SGIR-enhanced response of [Ca(2+)](i) to the activators of AC, PKA, and the L-type Ca(2+) channel in the myocytes isolated from the hearts subjected to SGIR. In conclusion, EA pretreatment can produce an antiarrhythmic effect in the rat of SGIR. AC, PKA and the L-type Ca(2+) channel are involved in the mediation of the antiarrhythmic effect of EA pretreatment.