Why the study?
Does adjusting external stimuli (acetylcholine, acid-base concentration, temperature) improve pacemaker function in a rabbit sinoatrial node model of sodium channel gene mutations?
Does adjusting external stimuli (acetylcholine, acid-base concentration, temperature) improve pacemaker function in a rabbit sinoatrial node model of sodium channel gene mutations?
Computational modeling demonstrates that abnormal pacemaker function caused by sodium channel mutations can be modulated and potentially recovered by adjusting external stimuli such as temperature and acid-base concentration.
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Hypothesis-generating for stimulus modulation in channelopathy models; leaves open translation to human pacemaker dysfunction.
Loss of function and gain of function mutations of the sodium channel were investigated using an intact two-dimensional rabbit sinoatrial node (SAN) and atrial cell model. The effects of three external stimuli (acetylcholine secretion by the vagal nerve, acid-base concentration, and tissue temperature) on cardiac pacemaker function and conduction were studied. Our results show that these two groups of mutations have different effects on pacemaker function and conduction. Furthermore, we found that the negative effects of these mutations could be altered by external stimuli. The bradycardic effects of mutations were magnified by an increase in acetylcholine level. Changes in acid-base concentration and tissue temperature increased the ability of the SAN to recover its pacemaker function. The results of this study increase our understanding of sodium channel disorders, and help to advance research on the treatment of these conditions.
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Zhang et al. (2013) studied this question.
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