The Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China.
Cardiovascular Research Institute, Wuhan University, Wuhan, PR China.
PLoS One. 2018 Aug 28;13(8):e0203083. doi: 10.1371/journal.pone.0203083. eCollection 2018.
Cardiac sympathetic tone overdrive is a key mechanism of arrhythmia. Cardiac sympathetic nerves denervation, such as LSG ablation or renal sympathetic denervation, suppressed both the prevalence of VAs and the incidence of SCD. Accumulating evidence demonstrates the ligament of Marshall (LOM) is a key component of the sympathetic conduit between the left stellate ganglion (LSG) and the ventricles. The present study aimed to investigate the roles of the distal segment of LOM (LOMLSPV) denervation in ischemia and reperfusion (IR)-induced VAs, and compared that LSG denervation. Thirty-three canines were randomly divided into group 1 (IR group, n = 11), group 2 (LOMLSPV Denervation + IR, n = 9), and group 3 (LSG Denervation + IR, n = 13). Hematoxylin-Eosin (HE) and Immunohistochemistry staining revealed that LOMLSPV contained bundles of sympathetic but not parasympathetic nerves. IR increased the cardiac sympathetic tone [serum concentrations of noradrenaline (NE) and epinephrine (E)] and induced the prevalence of VAs [ventricular premature beat (VPB), salvo of VPB, ventricular tachycardia (VT), VT duration (VTD) and ventricular fibrillation (VF)]. Both LOMLSPV denervation and LSG denervation could reduce the cardiac sympathetic tone in Baseline (BS) [heart rate variability (HRV)]. Compared with group 1, LOMLSPV denervation and LSG denervation similarly reduced sympathetic tone [NE (1.39±0.068 ng/ml in group 2, 1.29±0.081 ng/ml in group 3 vs 2.32±0.17 ng/ml in group 1, P<0.05) and E (114.64±9.22 pg/ml in group 2, 112.60±9.69 pg/ml in group 3 vs 166.18±15.78 pg/ml in group 1, P<0.05),] and VAs [VT (0±3.00 in group 2, 0±1.75 in group 3 vs 8.00±11.00 in group 1, P<0.05) and VTD (0 ± 4 s in group 2, 0±0.88s in group 3 vs 10.0 ± 22.00s in group 1, P<0.05)] after 2h reperfusion. These findings indicated LOMLSPV denervation reduced the prevalence of VT by suppressing SNS activity. These effects are comparable to those of LSG denervation. In myocardial IR, the anti-arrhythmic effects of LOMLSPV Denervation may be related to the inhibition of the expression of NE and E.
心脏交感神经亢进是心律失常的一个关键机制。心脏交感神经去神经支配，如 LSG 消融或肾交感神经去神经支配，抑制了室性心律失常（VA）的发生率和心源性猝死（SCD）的发生率。越来越多的证据表明，Marshall 韧带（LOM）是左星状神经节（LSG）和心室之间交感神经传导的关键组成部分。本研究旨在探讨 LO 的远段（LOMLSPV）去神经支配在缺血再灌注（IR）诱导的 VA 中的作用，并与 LSG 去神经支配进行比较。33 只犬随机分为 1 组（IR 组，n = 11）、2 组（LOMLSPV 去神经支配+IR，n = 9）和 3 组（LSG 去神经支配+IR，n = 13）。苏木精-伊红（HE）和免疫组织化学染色显示 LOMLSPV 包含束状交感神经，但不含副交感神经。IR 增加了心脏交感神经张力[血清去甲肾上腺素（NE）和肾上腺素（E）浓度]，并诱导了 VA 的发生率[室性早搏（VPB）、VPB 连发、室性心动过速（VT）、VT 持续时间（VTD）和心室颤动（VF）]。LOMLSPV 去神经支配和 LSG 去神经支配均可降低基础状态（BS）时的心脏交感神经张力[心率变异性（HRV）]。与第 1 组相比，LOMLSPV 去神经支配和 LSG 去神经支配相似地降低了交感神经张力[NE（第 2 组 1.39±0.068ng/ml，第 3 组 1.29±0.081ng/ml，第 1 组 2.32±0.17ng/ml，P<0.05）和 E（第 2 组 114.64±9.22pg/ml，第 3 组 112.60±9.69pg/ml，第 1 组 166.18±15.78pg/ml，P<0.05）]和 VA[VT（第 2 组 0±3.00，第 3 组 0±1.75，第 1 组 8.00±11.00，P<0.05）和 VTD（第 2 组 0±4s，第 3 组 0±0.88s，第 1 组 10.0±22.00s，P<0.05）]在再灌注 2h 后。这些发现表明，LOMLSPV 去神经支配通过抑制 SNS 活性降低了 VT 的发生率。这些作用与 LSG 去神经支配相当。在心肌 IR 中，LOMLSPV 去神经支配的抗心律失常作用可能与 NE 和 E 的表达抑制有关。
