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 β 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 SGIRenhanced 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.

Acupuncture Promotes Angiogenesis after Myocardial Ischemia through H3K9 Acetylation Regulation at VEGF Gene

“…The results suggested that EA treatment decreased ST segment change and Q-wave area, reduced the release of CK, LDH, and CK-MB from the necrosis heart tissue, and alleviated myocardial remodeling. These findings were consistent with previous studies [9]–[12].…”

“…Recently, acupuncture at the PC6 acupoint has been reported to attenuate cardiac injury, such as correcting arrhythmia, reducing apoptosis, and decreasing myocardial enzymes and infarction [9]–[12], which were induced by acute myocardial ischemia. However, the mechanism underlying the protective effects of acupuncture on MI remains unclear.…”

Involvement of mitochondrial permeability transition pore (mPTP) in cardiac arrhythmias: Evidence from cyclophilin D knockout mice

“…The definitions and point values of various arrhythmic events are as follows [25–27]: no arrhythmia: 0 points; PVC (one to three): 1 point; non-sustained VT (up to 10 beats): 2 points; sustained ventricular tachycardia: 3 points; ventricular fibrillation: 4 points. The highest scoring arrhythmogenic event from each heart was responsible for its score.…”

Electroacupuncture Pretreatment as a Novel Avenue to Protect Brain against Ischemia and Reperfusion Injury

“…Although protective mechanisms of EA pretreatment are largely unknown, a series of studies have shown that EA pretreatment primarily regulates oxidative stress [49], maintains the integrity of blood-brain barrier (BBB) [40], and inhibits apoptosis [30, 33] via different receptors, for example, adenosine receptor type 1 (A1R) [11], opiod receptors [37], cannabinoid receptors (CB1, CB2) [41–44], N-methyl-d-aspartate receptors (NMDARs) [39], and downstream intracellular signaling events including K ATP channels [30], extracellular regulated kinase (ERK) [42], epsilon protein kinase C ( ε PKC) [44], and phosphatidylinositol 3-kinase (PI3K) pathway [50], while the researches of myocardial protective mechanisms induced by EA pretreatment mainly focus on β -adrenoreceptor ( β -AR) and postreceptor signaling pathway [34–36, 38, 51]. Signaling pathways involved in the neuroprotection of EA pretreatment were summarized in Figure 2.…”