title: Low-frequency extracellular potentials recorded from the sinoatrial node.
abstract: 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 (0.5-32 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 microV 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 microM 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 microM 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Humoral Regulation, Nagoya University, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Yamamoto
authors.forename: H
authors.initials: H
authors.lastname: Honjo
authors.forename: R
authors.initials: R
authors.lastname: Niwa
authors.forename: I
authors.initials: I
authors.lastname: Kodama
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002304:Cardiac Pacing, Artificial; D004558:Electric Stimulation; D004594:Electrophysiology; D005110:Extracellular Space / Q000187:drug effects / Q000502:physiology*; D006325:Heart Atria; D008564:Membrane Potentials / Q000187:drug effects; D008839:Microelectrodes; D009543:Nifedipine / Q000494:pharmacology; D010477:Perfusion; D011817:Rabbits; D012849:Sinoatrial Node / Q000187:drug effects / Q000502:physiology*; D026941:Sodium Channel Blockers; D013779:Tetrodotoxin / Q000494:pharmacology; D014630:Vagus Nerve
chemical_list: D002121:Calcium Channel Blockers; D026941:Sodium Channel Blockers; D013779:Tetrodotoxin; D009543:Nifedipine