Cai Jie, Tang Min, Liu Hao, Ding Shiao, Lu Rongxin, Wang Wei, Ma Nan, Mei Ju, Jiang Zhaolei
Department of Cardiothoracic Surgery, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200092, China.
Cardiol Res Pract. 2021 Feb 2;2021:8869264. doi: 10.1155/2021/8869264. eCollection 2021.
The purpose is to observe the effects and neural mechanism of cutting upper thoracic sympathetic trunk (TST) on the ventricular rate (VR) during persistent atrial fibrillation (AF).
Twelve beagle dogs were halving to the control group and experimental group, 6 dogs for each group. Both groups were performed with left atrial rapid pacing (600 beats/min) to induce sustained AF. The experimental group underwent cutting upper TST after a sustained AF model was established, while the control group received thoracotomy without cutting TST. Bilateral stellate ganglion (SG) and left atrial myocardium were harvested for tyrosine-hydroxylase (TH) immunohistochemical staining.
After cutting upper TST for 30 minutes, the average VR was 121.5 ± 8.7 bpm (95% CI, 114.8 to 128.0) in the experimental group, which was significantly slower than that of the control group (144.5 ± 4.2 bpm (95% CI, 141.5 to 148.0)) ( < 0.001). After cutting upper TST for 1 month, the average VR of the experimental group (106.5 ± 4.9 bpm (95% CI, 102.0 to 110.0)) was also significantly slower versus that of the control group (139.2 ± 5.6 bpm (95% CI, 135.0 to 143.8)) ( < 0.001). Compared with the control group, both left stellate ganglion (LSG) and right stellate ganglion (RSG) of the experimental group caused neural remodeling characterized by decreased ganglionic cell density and reduced TH staining. TH-positive component was significantly decreased in the left atrium of the experimental group compared with the control group.
Cutting upper TST could reduce fast VR during persistent AF. Cutting upper TST induced bilateral SG neural remodeling and reduced sympathetic nerve density in the left atrium, which could contribute to the underlying mechanism of VR control during AF.
观察切断上胸段交感神经干（TST）对持续性心房颤动（AF）时心室率（VR）的影响及其神经机制。
将12只比格犬分为对照组和实验组，每组6只。两组均行左心房快速起搏（600次/分钟）以诱发持续性AF。实验组在建立持续性AF模型后切断上胸段TST，而对照组仅行开胸手术但不切断TST。采集双侧星状神经节（SG）和左心房心肌进行酪氨酸羟化酶（TH）免疫组化染色。
切断上胸段TST 30分钟后，实验组平均VR为121.5±8.7次/分钟（95%CI，114.8至128.0），显著慢于对照组（144.5±4.2次/分钟（95%CI，141.5至148.0））（P<0.001）。切断上胸段TST 1个月后，实验组平均VR（106.5±4.9次/分钟（95%CI，102.0至110.0））也显著慢于对照组（139.2±5.6次/分钟（95%CI，135.0至143.8））（P<0.001）。与对照组相比，实验组左星状神经节（LSG）和右星状神经节（RSG）均出现神经重塑，表现为神经节细胞密度降低和TH染色减少。实验组左心房TH阳性成分较对照组显著减少。
切断上胸段TST可降低持续性AF时的快速VR。切断上胸段TST可诱导双侧SG神经重塑并降低左心房交感神经密度，这可能是AF时控制VR的潜在机制。
