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Cardiovascular Research 1998 39(2):360-372; doi:10.1016/S0008-6363(98)00091-1
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Low-frequency extracellular potentials recorded from the sinoatrial node

Mitsuru Yamamoto, Haruo Honjo, Ryoko Niwa and Itsuo Kodama*

Department of Humoral Regulation, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-01, Japan

* Corresponding author. Tel.: +81 (52) 789 5007; Fax: +81 (52) 789 5003; e-mail: ikodama@endeavor.riem.nagoya-u.ac.jp

Objective: To study the morphology of small extracellular potentials localized to the sinoatrial (SA) node and to elucidate its potential usefulness in evaluating SA node dysfunction. Methods: Extracellular potentials were recorded from the endocardial surface of the SA node in isolated right atrial preparations of rabbits through custom-made modified bipolar electrodes with high-gain amplification and a low-frequency (0.5–30 Hz) filter setting. Results: The potentials in and around the SA node under control conditions showed a variety of morphologies. In a small area near the leading pacemaker site, slow primary negative deflections were preceded by a gradual increase of the negativity (73.5±5.6 µV in amplitude, n=12). In the periphery of the SA node cranial and caudal to the leading pacemaker site, slow positive/negative deflections were recorded. In the septal side of the SA node showing very slow conduction, the electrograms showed slow primary positive deflections. Transient pacemaker shifts induced by atrial stimulation or vagal nerve stimulation were reflected well in morphologies of the extracellular potentials. In the presence of 20 µM TTX, wide and slow negative deflections were observed in the center and periphery of the SA node in association with extremely slow conduction restricted to a corridor-like area along the crista terminalis, whereas the atrial muscle surrounding the area was made inexcitable. In the presence of 1 µM nifedipine, the leading pacemaker site was shifted to the periphery of the SA node close to the crista terminalis. The negative deflection in the center and septal side of the SA node disappeared reflecting no excitation of the area. Conclusion: The endocardial extracellular electrograms recorded in and around the SA node under appropriate conditions reflect two dimensional activation sequences. They would provide useful information in recognizing the leading pacemaker site and alterations of the conductivity and excitability.

KEYWORDS Sinoatrial node; Extracellular potentials; Transmembrane potentials; Tetrodotoxin; Nifedipine


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