Japanese Journal of Electrocardiology
Online ISSN : 1884-2437
Print ISSN : 0285-1660
ISSN-L : 0285-1660
Volume 35, Issue 4
Displaying 1-13 of 13 articles from this issue
  • Shingo Murakami, Atsushi Inanobe, Yoshihisa Kurachi
    2016Volume 35Issue 4 Pages 245-257
    Published: 2016
    Released on J-STAGE: March 25, 2016
    JOURNAL FREE ACCESS
    Acetylcholine (ACh) increases the amplitude of cardiac K+ current (IK.ACh) through activation of the muscarinic K+ (KACh) channel, but the amplitude gradually decreases to a quasi-steady-state level within seconds. This phenomenon, known as short-term desensitization, is believed to play a role in cellular adaptation to external input. However, the precise mechanism and physiological role of short-term desensitization is still unclear. In the present review, we introduced our experimental and theoretical studies on the mechanisms underlying short-term desensitization of IK.ACh. In atrial myocytes, short-term desensitization features the unique dose responses of the transient and quasi-steady state IK.ACh, effects of ACh preperfusion and recovery from short-term desensitization. In simulation analysis, two conditions are required for the mathematical IK.ACh model to reconstitute short-term desensitization. The first condition is distinct muscarinic receptors (M2Rs) with different affinities for ACh, which conferred an IK.ACh response over a wide range of ACh concentrations. The second condition is 2 distinct KACh channels with different affinities for the G-proteinβγsubunit, which contributes to reconstitution of the temporal behavior of IK.ACh. Under these conditions, the model quantitatively reproduced the unique properties of short-term desensitization observed in experiments. Furthermore, the present model conferred vagal escape on the mathematical action potential models of sinus node cells. Therefore, 2 different populations of KACh channels and M2Rs may be responsible for short-term desensitization and vagal escape at nodal cells.
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  • Seiko Mizuno, Masaki Matsunaga, Yusaku Mochizuki, Kazue Yaginuma, Keis ...
    2016Volume 35Issue 4 Pages 258-263
    Published: 2016
    Released on J-STAGE: March 25, 2016
    JOURNAL FREE ACCESS
    We report a case of atrial tachycardia due to pregnancy. A 37 years old woman was admitted to our hospital for the treatment of palpitation. She was aware of palpitation from the 15th week of pregnancy, but her condition was diagnosed as sinus tachycardia. The electrocardiogram on admission showed long RP'tachycardia (170/min), which was difficult to terminate with ATP, Pilsicainide and Verapamil. β blocker was effective with this patient, and she was able to give birth at 38weeks of pregnancy without any difficulties. Atrial tachycardia has not recurred. The exact mechanism of increased arrhythmia burden during pregnancy is unclear, but has been attributed to autonomic changes related to pregnancy. We concluded that a β blocker was effective in this case.
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