医学
星状神经节
心肌梗塞
心脏病学
内科学
刺激
交感神经系统
结扎
麻醉
病理
血压
替代医学
作者
Chunrong Xiang,Cheng Yang,Xiaomei Yu,Tianlong Mao,Hui Luo,Hao‐Yuan Hu,Yuzhe Wu,R. T. Sang,Zhuo Wang,Yujie Wang,Qinyu Luo,Jingyu Huang,Jun Zhao,Jiale Wang,Xinqi Wang,Mingxian Chen,Wei Liu,Liping Zhou,Songyun Wang,Hong Jiang
出处
期刊:Heart Rhythm
[Elsevier]
日期:2024-03-01
卷期号:21 (3): 340-348
标识
DOI:10.1016/j.hrthm.2023.11.026
摘要
Our previous study showed that light-emitting diode modulation of the hypothalamic paraventricular nucleus (PVN), which is the control center of the sympathetic nervous system, might attenuate neuroinflammation in the PVN and prevent ventricular arrhythmias (VAs) after myocardial infarction (MI). Low-intensity focused ultrasound (LIFU) has deeper penetration than does light-emitting diode, while its effect on the PVN has not been reported.This study aimed to explore the effect of LIFU modulation of the PVN on the inducibility of post-MI VAs.Fifty-four Sprague-Dawley rats were randomly divided into acute control (n = 12, 22.22%), acute MI (AMI, n = 12, 22.22%), AMI + LIFU (n = 12, 22.22%), chronic control (n = 6, 11.11%), chronic MI (CMI, n = 6, 11.11%), and CMI + LIFU (n = 6, 11.11%) groups. MI was induced by left anterior artery ligation, and electrocardiographic recording for 0.5 hours after MI and programmed electrophysiological stimulation were used to test the vulnerability of VAs. Peripheral sympathetic neural activity was assessed by measuring left stellate ganglion neural activity. Finally, hearts and brains were extracted for Western blotting and histopathological analysis, respectively.Compared with the AMI group, AMI-induced VAs (P < .05) and left stellate ganglion neural activity (P < .05) were significantly attenuated in the AMI + LIFU group. In addition, LIFU resulted in a significant reduction of microglial activation in the PVN and expression of inflammatory cytokines in the peri-ischemic myocardium. In the CMI + LIFU group, there was no obvious tissue damage in the brain.LIFU modulation of the PVN may prevent the incidence of post-MI VAs by attenuating MI-induced sympathetic neural activation and inflammatory response.
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