Abstract
Abstract
Background
Renal denervation (RDN) can reduce ventricular arrhythmia after acute myocardial infarction (AMI), but the mechanism is not clear. The purpose of this study is to study its mechanism.
Methods
Thirty-two Sprague–Dawley rats were divided into four groups: control group, AMI group, RDN-1d + AMI group, RDN-2w + AMI group. The AMI model was established 1 day after RDN in the RDN-1d + AMI group and 2 weeks after RDN in the RDN-2w + AMI group. At the same time, 8 normal rats were subjected to AMI modelling (the AMI group). The control group consisted of 8 rats without RDN intervention or AMI modelling.
Results
The study confirmed that RDN can reduce the occurrence of ventricular tachycardia in AMI rats, reduce renal sympathetic nerve discharge, and inhibit the activity of local sympathetic nerves and cell growth factor (NGF) protein expression in the heart after AMI. In addition, RDN decreased the expression of norepinephrine (NE) and glutamate in the hypothalamus,and NE in cerebrospinal fluid, and increased the expression level of γ aminobutyric acid (GABA) in the hypothalamus after AMI.
Conclusion
RDN can effectively reduce the occurrence of ventricular arrhythmia after AMI, and its main mechanism may be via the inhibition of central sympathetic nerve discharge.
Funder
The Shanghai Key Medical Specialties Construction Project
Health System Independent Innovation Science Foundation of Shanghai Putuo District
Science and Technology Innovation Plan Of Shanghai Science and Technology Commission
Shanghai Municipal Health and Health Commission Health Industry Clinical Research Project
Young Elite Scientists Sponsorship Program by CAST
Publisher
Springer Science and Business Media LLC
Subject
Cardiology and Cardiovascular Medicine
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