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Increase of Autonomic Nerve Factors in Epicardial Ganglionated Plexi During Rapid Atrial Pacing Induced Acute Atrial Fibrillation.

BACKGROUND The cardiac autonomic nervous system plays an essential role in epicardial ganglionated plexi (GP) regulation of atrial fibrillation onset and progression. To date, the activity of GP and the function of the cardiac autonomic nervous system are not well understood. The aim of this study was to determine alterations in epicardial GP cholinergic nerve, adrenergic nerve, and nerve growth factor expression using rapid atrial pacing to induce atrial fibrillation in canines. MATERIAL AND METHODS Nine healthy adult beagles were divided into two groups: the pacing experimental group (n=6) and the sham-operation control group (n=3). For the pacing group, high frequency pacing of the left atrial appendage was performed for eight hours. In the control group, electrodes were implanted without rapid atrial pacing. Immunocytochemistry was used to identify neurons positively expressing tyrosine hydroxylase, choline acetyl transferase, nerve growth factor and neurturin. RESULTS After successfully establishing a rapid atrial pacing of the left atrial appendage induced atrial fibrillation model, we found that expression of choline acetyl transferase, tyrosine hydroxylase, nerve growth factor, and neurturin was significantly higher in the rapid atrial pacing group than the control group (p<0.05). CONCLUSIONS In our model, incremental excitability of both the adrenergic and cholinergic nerves led to frequent incidents of atrial fibrillation, which were possibly due to an imbalance of autonomic nerve factors in the epicardial GP during acute atrial fibrillation.

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