Department of Cardiac Pacing and Electrophysiology, Heart Center, First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China (mainland).
Department of Critical Care Medicine, Fifth Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China (mainland).
Med Sci Monit. 2020 May 24;26:e922277. doi: 10.12659/MSM.922277.
BACKGROUND Imbalanced cardiac autonomic control and cardiac receptors redistribution contribute to the arrhythmogenic substrate under the myocardial infarction (MI) condition. Stimulating the auricular branch of vagus nerve (AB-VNS) has been proven to reduce post-infarction ventricular arrhythmia (VAs), but its potential mechanisms were largely unknown. This study aimed to investigate whether long-term intermittent low-intensity AB-VNS could produce a protective effect on modulating autonomic activities and abnormal redistribution of autonomic nerve efferent receptors in a MI canine model. MATERIAL AND METHODS Twelve healthy beagle dogs underwent ligation of the left anterior descending coronary artery to establish a MI model and were randomized into 2 groups: an AB-VNS group, (AB-VNS for 4 weeks) and a control group (sham stimulation for 4 weeks). Dynamic electrocardiogram recording, neural recording, catecholamine concentration, and histological studies were conducted subsequently. RESULTS Compared to the control group, the AB-VNS group had significantly suppressed post-infarction VAs, reduced low frequency (LF) power and increased high frequency (HF) power. In the AB-VNS group, with the progression of reduced cardiac sympathetic activities and augmented cardiac parasympathetic activities, the catecholamine concentration in heart tissue declined in the peripheral infarction area and right ventricle (RV); tyrosine hydroxylase (TH)-positive neurons decreased in the inferior cardiac sympathetic nerve, and choline acetyltransferase (ChAT)-positive neurons increased in the cervical vagus nerve. Expression of TrkA and P75NGFR were reduced in the peripheral MI (peri-MI) and non-MI area with AB-VNS. The mRNA expression of adrenergic and nicotinic receptors (ß₁-AR, ß₃-AR, and CHRNA7) significantly declined in the peri-MI and non-MI area of the AB-VNS group. CONCLUSIONS Chronic intermittent low-intensity AB-VNS effectively suppressed post-infarction VAs by potentially rebalancing extracardiac intrathoracic autonomic activities, reducing excessive cardiac sympathetic denervation, and attenuating the heterogeneities of cardiac efferent nerve receptors distribution.
心脏自主神经控制失衡和心脏受体再分布是心肌梗死后心律失常发生的基质。刺激迷走神经耳支（AB-VNS）已被证明可减少梗死后室性心律失常（VAs），但其潜在机制尚不清楚。本研究旨在探讨长期间歇性低强度 AB-VNS 是否能对调节自主活动和异常分布的自主神经传出受体产生保护作用，从而在犬心肌梗死模型中建立一个保护作用。
12 只健康比格犬行左前降支冠状动脉结扎术，建立心肌梗死模型，随机分为 2 组：AB-VNS 组（AB-VNS 治疗 4 周）和对照组（假刺激 4 周）。随后进行动态心电图记录、神经记录、儿茶酚胺浓度和组织学研究。
与对照组相比，AB-VNS 组梗死后 VAs 明显减少，低频（LF）功率降低，高频（HF）功率增加。在 AB-VNS 组，随着心脏交感神经活动的降低和心脏副交感神经活动的增强，心脏组织中的儿茶酚胺浓度在周围梗死区和右心室（RV）降低；下心脏交感神经中的酪氨酸羟化酶（TH）阳性神经元减少，颈迷走神经中的胆碱乙酰转移酶（ChAT）阳性神经元增加。AB-VNS 组周围心肌梗死（peri-MI）和非心肌梗死区的 TrkA 和 P75NGFR 表达减少。peri-MI 和非心肌梗死区的肾上腺素能和烟碱型受体（ß₁-AR、ß₃-AR 和 CHRNA7）的 mRNA 表达显著下降。
慢性间歇性低强度 AB-VNS 通过潜在地重新平衡胸外胸腔自主活动，减少过度的心脏交感神经去神经支配，减轻心脏传出神经受体分布的异质性，有效抑制梗死后 VAs。
