| Objective:To investigate the effects and mechanism of renal denervation(RDN)on ventricular arrhythmia after acute myocardial infarction(AMI).Methods:Using a rat myocardial infarction model,24 Sprague-Dawley(SD)rats were divided into four groups,the control group(n=6),the AMI group(n=6),and the RDN-1d+AMI group(n=6),RDN-2w+AMI group(n=6),SD rats were first subjected to RDN intervention,and the rats were reared separately according to the above groups.Rats in the RDN-1d+AMI group were raised for 1 day to establish an AMI model.In the RDN-2w+AMI group was fed for 2 weeks and then AMI modeled.At the same time,AMI modeling was performed on 6normal rats,namely the AMI group,and 6 rats in the control group were not subjected to RDN intervention and AMI modeling.Power Lab multi-channel ECG monitor was continuously recorded after surgery to monitor the inhibitory effect of RDN on the occurrence of ventricular arrhythmia.After 1 hour of observation,the renal arteries and peripheral sympathetic nerves were detected by HE staining to evaluate the effectiveness of RDN,TH staining was used to detect cardiac sympathetic nerve activity,and the degree of myocardial fibrosis was detected by Masson staining.Western blot(WB)was used to detect the protein expression levels of Cav1.2,Nav1.5 and Kir2.1 of various ion channels in myocardial infarction area.Renal sympathetic nerve activity was detected by Power Lab/8SP biological information acquisition instrument.Enzyme-linked immunosorbent assay(ELISA)was used to detect the expression of brain natriuretic peptide(BNP),norepinephrine(NE)and creatinine(Cr).Results:Compared with the AMI group(331.2±74.8),the number of ventricular tachycardia was significantly reduced in the RDN-1d+AMI group(112±59.2,P<0.001)and the RDN-2w+AMI group(151±87.9,P=0.003),and the number of reductions was more pronounced in the RDN-1d group.Compared with the sympathetic nerve discharge in the Control group(11.9±0.6),the RDN-1d group(6.6±1.7,P<0.001)and the RDN-2w group(8.0±2.8,P=0.033)significantly decreased,with the RDN-1d group showing a more significant effect.TH staining suggested that RDN might inhibit local sympathetic nerve activity after AMI,and Masson staining indicated that four groups of rats had not yet developed cardiac fibrosis.Compared with the control group,the protein expressions of Nav1.5,Cav1.2 and Kir2.1 in the AMI group were significantly down-regulated,while the RDN-2w+AMI group inhibited the down-regulated protein expressions of Nav1.5,Cav1.2and Kir2.1 in the AMI group,while the RDN-1d+AMI group cannot inhibit the down-regulation of protein expression.Compared with the BNP and NE in the control group,the levels of BNP and NE in the AMI group were significantly increased(P<0.001).Compared with the AMI group,the BNP and NE in the RDN-1d+AMI group and the RDN-2w+AMI group had no significant changes(P>0.05),showing no statistical significance.There was no significant difference in the expression levels of Cr in the four groups of rats.Conclusion:RDN can effectively reduce the occurrence of ventricular arrhythmias after AMI.In the early stage,it mainly inhibits renal sympathetic nerve discharge,and later inhibits renal sympathetic discharge and ion channel protein upregulation. |
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