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

  • Gao Junhong
    Department of Physiology, Institute of Acupuncture, China Academy of Chinese Medical Sciences
  • Zhang Ling
    Department of Pharmacology, Liaoning Medical College, China Academy of Chinese Medical Sciences
  • Wang Yumin
    Department of Pharmacology, Liaoning Medical College, China Academy of Chinese Medical Sciences
  • Lu Bo
    Department of Physiology, Experimental Research Center, China Academy of Chinese Medical Sciences
  • Cui Haifeng
    Department of Physiology, Experimental Research Center, China Academy of Chinese Medical Sciences
  • Fu Weixing
    Department of Physiology, Institute of Acupuncture, China Academy of Chinese Medical Sciences
  • Wang Hongxin
    Department of Pharmacology, Liaoning Medical College, China Academy of Chinese Medical Sciences
  • Yu Youhua
    Department of Physiology, Experimental Research Center, China Academy of Chinese Medical Sciences
  • Yu Xiaochun
    Department of Physiology, Experimental Research Center, China Academy of Chinese Medical Sciences

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タイトル別名
  • 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

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説明

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 Ca2+ channel, theβ1-AR signaling components modulating intracellular Ca2+ ([Ca2+]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 [Ca2+]i to the activators of AC, PKA, and L-type Ca2+ 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 [Ca2+]i to the activators of AC, PKA, and the L-type Ca2+ 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 Ca2+ channel are involved in the mediation of the antiarrhythmic effect of EA pretreatment. <br>

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