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Pacemaker Shift in the Rabbit Sinoatrial Node in Response to Vagal Nerve Stimulation
Author(s) -
Shibata Nitaro,
Inada Shin,
Mitsui Kazuyuki,
Honjo Haruo,
Yamamoto Mitsuru,
Niwa Ryoko,
Boyett Mark R.,
Kodama Itsuo
Publication year - 2001
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/eph8602100
Subject(s) - crista terminalis , sinoatrial node , stimulation , beat (acoustics) , vagus nerve , heart rate , cardiology , chemistry , anatomy , medicine , biology , physics , blood pressure , atrial fibrillation , catheter ablation , acoustics
Effects of brief postganglionic vagal nerve stimulation on the activation sequence of the rabbit sinoatrial (SA) node were investigated. Activation sequences in a small area (7 mm × 7 mm) on the epicardial surface were measured in a beat‐to‐beat manner using an extracellular potential mapping system composed of 64 modified bipolar electrodes with high‐gain and low‐frequency band‐pass filtering. The leading pacemaker site was recognised clearly from both the activation sequence and the characteristic morphology of the potentials. Vagal stimulation resulted in a short‐lasting initial slowing of spontaneous rate followed by a long‐lasting secondary slowing; a brief period of relative or absolute acceleration was interposed between the two slowing phases. During these changes of spontaneous rate, the leading pacemaker site shifted in a complex beat‐to‐beat manner by 1‐6 mm alongside the crista terminalis in the superior or inferior direction. For the first spontaneous excitation following stimulation, the greater the slowing, the larger the distance of the pacemaker shift. There was no such linear relationship between the extent of slowing and the distance of pacemaker shift for the subsequent beats. These changes in the leading pacemaker site in response to vagal stimulation may be the result of the functional and morphological heterogeneity of the mammalian SA node in terms of innervation, receptor distribution and ion channel densities.