Sun Juan, Lu Yanmei, Wugeti Najina, Aikemu Ainiwaer
Heart Center, The First Affiliated Hospital of Xinjiang Medical University Urumqi 830054, Xinjiang, China.
Department of Drug Analysis, Faculty of Pharmacy, Xinjiang Medical University Urumqi 830011, Xinjiang, China.
Int J Clin Exp Med. 2015 Apr 15;8(4):4968-78. eCollection 2015.
This study sought to examine the effect of the cardiac autonomic nerve plexus, which originates from the vagus nerve trunk, on atrial vulnerability.
Dogs in group I (n = 6) underwent ganglionated plexi (GP) sequential ablation following six hours of left atrial appendage rapid atrial pacing (RAP). The monophasic action potential duration at 90% of repolarization (APD90), effective refractory period (ERP), and the atrial fibrillation inducing rate of bilateral atria and pulmonary veins were recorded at baseline, l h, 3 h and 6 h after pacing, as well as after sequential ablation (RAGP + RIGP ablation, LSGP + RIGP ablation). Dogs in group II (n = 6) received vagus nerve stimulation following six hours of left atrial appendage RAP. APD90, ERP and atrial fibrillation inducing rate of bilateral atria and pulmonary veins were recorded at baseline, 1 h, 3 h and 6 h after pacing, as well as after GP sequential ablation (RAGP + RIGP ablation, LSGP + RIGP ablation).
In group I, APD90 and ERP progressively shortened and atrial fibrillation inducing rate increased in various sites l h, 3 h and 6 h after RAP (P < 0.05). APD90 and ERP shortened significantly and atrial fibrillation inducing rate was significantly higher in the left atrial appendage and bilateral pulmonary veins than in other sites (P < 0.05). Following GP sequential ablation, APD90, ERP and atrial fibrillation inducing rate were not significantly different from baseline levels (P > 0.05). In group II, APD90 and ERP progressively shortened in various sites over pacing time period, and the atrial fibrillation inducing rate increased l h, 3 h and 6 h after RAP + VNS (P < 0.05). APD90 and ERP shortened significantly and atrial fibrillation inducing rate was significantly higher in the left atrial appendage and right superior/inferior pulmonary veins when compared with other sites (P < 0.05). After GP sequential ablation, APD90, ERP and atrial fibrillation inducing rate were not significantly different from baseline levels (P > 0.05). Compared with group I, APD90 and ERP shortened significantly, while atrial fibrillation inducibility increased significantly at baseline and l h, 3 h, and 6 h after pacing in group II (P < 0.05). After ablation of the four major cardiac GPs, no significant differences were observed in the two groups with respect to APD90, ERP and atrial fibrillation inducing rate (P > 0.05).
GP activation, as a result of vagal nerve stimulation, alters MAP90, ERP and atrial fibrillation inducing rate of the atrium and pulmonary veins and promotes the occurrence of RAF in the early stage of atrial fibrillation, resulting in increased atrial vulnerability and triggering the occurrence and maintenance of atrial fibrillation.
本研究旨在探讨源自迷走神经干的心脏自主神经丛对心房易损性的影响。
第一组（n = 6）的犬在左心耳快速心房起搏（RAP）6小时后进行神经节丛（GP）顺序消融。在起搏前基线、起搏后1小时、3小时和6小时以及顺序消融后（右心房神经节丛+右肺静脉神经节丛消融、左心房上神经节丛+右肺静脉神经节丛消融）记录复极化90%时的单相动作电位时程（APD90）、有效不应期（ERP）以及双侧心房和肺静脉的房颤诱发率。第二组（n = 6）的犬在左心耳RAP 6小时后接受迷走神经刺激。在起搏前基线、起搏后1小时、3小时和6小时以及GP顺序消融后（右心房神经节丛+右肺静脉神经节丛消融、左心房上神经节丛+右肺静脉神经节丛消融）记录APD90、ERP以及双侧心房和肺静脉的房颤诱发率。
在第一组中，RAP后1小时、3小时和6小时，各部位的APD90和ERP逐渐缩短，房颤诱发率增加（P < 0.05）。左心耳和双侧肺静脉的APD90和ERP显著缩短，房颤诱发率显著高于其他部位（P < 0.05）。GP顺序消融后，APD90、ERP和房颤诱发率与基线水平无显著差异（P > 0.05）。在第二组中，在起搏时间段内各部位的APD90和ERP逐渐缩短，RAP + 迷走神经刺激后1小时、3小时和6小时房颤诱发率增加（P < 0.05）。与其他部位相比，左心耳和右上/下肺静脉的APD90和ERP显著缩短，房颤诱发率显著更高（P < 0.05）。GP顺序消融后，APD90、ERP和房颤诱发率与基线水平无显著差异（P > 0.05）。与第一组相比，第二组在起搏前基线、起搏后1小时、3小时和6小时时APD90和ERP显著缩短，而房颤诱发能力显著增加（P < 0.05）。在消融四个主要心脏GP后，两组在APD90、ERP和房颤诱发率方面未观察到显著差异（P > 0.05）。
迷走神经刺激导致的GP激活改变了心房和肺静脉的MAP90、ERP和房颤诱发率，并在房颤早期促进了RAF的发生，导致心房易损性增加，触发房颤的发生和维持。
