医学
微量注射
心脏病学
内科学
心功能曲线
心肌梗塞
神经节
麻醉
交感神经系统
心室重构
心力衰竭
血压
解剖
作者
Song Zhang,Meng Wang,Liying Jiao,Chengzhe Liu,Huaqiang Chen,Liping Zhou,Yueyi Wang,Yuhong Wang,Lei Zhu,Zihan Liu,Yuyang Zhou,Huixin Zhou,Xiao Xu,Zeyan Li,Lei Zhu,Zhongyang Yu,Liqing Nie,Lilei Yu,Hong Jiang
出处
期刊:Heart Rhythm
[Elsevier]
日期:2022-08-07
卷期号:19 (12): 2095-2104
被引量:11
标识
DOI:10.1016/j.hrthm.2022.08.002
摘要
Strategies to improve various cardiovascular diseases by blocking cardiac sympathetic ganglion have been increasingly available currently. Botulinum toxin type A (BTA), a typical neurotoxin, has been shown to block neural transmission in a safe and long-lasting manner.The aim of the present preclinical study was to assess the efficacy of BTA microinjection to alleviate cardiac remodeling after chronic myocardial infarction (MI) by blocking cardiac sympathetic ganglion in a canine model.Beagles were randomly divided into a control group (saline microinjection with sham surgery), an MI group (saline microinjection with MI), and an MI + BTA group (BTA microinjection with MI). Ultrasound-guided percutaneous BTA or saline injection into the left stellate ganglion (LSG) was performed followed by MI induction via left anterior descending artery occlusion (LADO) or sham surgery. After 30 days, electrocardiography, Doppler echocardiography, LSG function, neural activity, and ventricular electrophysiological detection were performed in all experimental dogs. At the end, LSG and ventricular tissues were collected for further detection.BTA treatment significantly inhibited LSG function and neural activity and improved heart rate variability. Additionally, BTA application alleviated ventricular remodeling, ameliorated cardiac function, and prevented ventricular arrhythmias after 30-day chronic LADO-induced MI.Ultrasound-guided percutaneous microinjection of BTA can block cardiac sympathetic ganglion to improve cardiac remodeling in a large animal model of chronic LADO-induced MI. Ultrasound-guided BTA microinjection has potential for clinical application as a novel cardiac sympathetic ganglion blockade strategy for MI.
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