Low-level ganglionated plexus stimulation facilitates atrial fibrillation: in vivo and in vitro studies

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• 作者：Liu Wu¹ ; Zhibing Lu¹ ; Hong Jiang ; ^{jianghong58@gmail.com} ; Bo He ; Wenbo He ; Bo Cui ; Xiaorong Hu ; Congxin Huang
• 关键词：Atrial fibrillation ; Autonomic nervous system ; Ganglionated plexus
• 刊名：Autonomic Neuroscience
• 出版年：2012
• 出版时间：21 May, 2012
• 年：2012
• 卷：168
• 期：1-2
• 页码：58-65
• 全文大小：777 K

文摘

Objectves

The purpose of the present study was to investigate whether long term low level autonomic activation can form electrophysiological substrate for atrial fibrillation (AF).

Methods and results

In 16 anesthetized open-chest dogs, electrodes on the anterior right ganglionated plexuses (GP) and superior left GP allowed 6-h low-level GP stimulation (LL-GPS) inducing a 10 % decrease in sinus rate. Similar low-level stimulation (without myocardial capture) was delivered to the myocardium remote from the GP for 6 h in another 16 dogs as control group. LL-GPS: a) induced shortening of the atrial effective refractory period and increase of the window of vulnerability for AF; b) significantly increased acetylcholine-regulated potassium current (I_KACh) at left superior pulmonary vein (LSPV) while reduced the density of L-type calcium current (I_CaL) at LSPV and both atria, the protein expression of the channel subunit showed a consistent alteration, however both without significant changes in mRNA level.

Conclusions

Six-hour LL-GPS induced significant changes in atrial electrophysiology and facilitated the initiation of AF, indicating that long-term low level autonomic activation would form electrophysiological substrate for AF. The underlying mechanism may be associated with a post-transcriptional regulation of increased I_KACh and decreased I_CaL.