Key result
Low temperature and the I(f) selective blocker ivabradine both caused a shift of the pacemaker within the rabbit sinoatrial node region.
Low temperature and ivabradine induce pacemaker shift in the rabbit sinoatrial node, with cholinergic inexcitability via I(KACh) activation identified as a key mechanism during acetylcholine exposure.
Hypothesis-generating for SAN pacemaker shifts; extends rabbit models but leaves open human translation or ivabradine implications.
Changes of the activation sequence in the rabbit sinoatrial node under the influence of low temperature and I(f) selective blocker ivabradine have been studied using the optical mapping technique. Both factors caused a shift of the pacemaker within the sinoatrial node region. These results are compared with the data obtained recently in the investigation of pacemaker shift under the influence of cholinergic and adrenergic factors. Possible mechanisms of the pacemaker shift are discussed. The suppression of electric activity in the central part of the sinoatrial node during the action of acetylcholine, which is called cholinergic inexcitability, may be considered as one of the mechanisms of the pacemaker shift. It is shown that the main cause of cholinergic inexcitability is the activation of potassium acetylcholine-dependent current I(KACh).
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Abramochkin et al. (2010) studied Pacemaker shift in the sinoatrial node. Low temperature and ivabradine was evaluated on Pacemaker shift within the sinoatrial node region. Low temperature and the I(f) selective blocker ivabradine both caused a shift of the pacemaker within the rabbit sinoatrial node region.
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