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Semaphorin 3a transfection into the left stellate ganglion reduces susceptibility to ventricular arrhythmias after myocardial infarction in rats

机译:Semaphorin 3a转染至左星状神经节可降低大鼠心肌梗死后对室性心律失常的敏感性

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摘要

Aims Myocardial infarction (MI) induces neural remodelling of the left stellate ganglion (LSG), which may contribute to ischaemia- induced arrhythmias. The neural chemorepellent Semaphorin 3a (Sema3a) has been identified as a negative regulator of sympathetic innervation in the LSG and heart. We previously reported that overexpression of Sema3a in the border zone could reduce the arrhythmogenic effects of cardiac sympathetic hyperinnervation post-MI. This study investigated whether Sema3a overexpression within the LSG confers an antiarrhythmic effect after MI through decreasing extra-and intra-cardiac neural remodelling.
机译:目的心肌梗死(MI)诱导左星状神经节(LSG)的神经重塑,这可能导致局部缺血性心律失常。神经化学趋化药Semaphorin 3a(Sema3a)已被确定为LSG和心脏交感神经支配的负调节剂。我们以前曾报道过,边界区Sema3a的过度表达可减少MI后心脏交感神经过度神经支配的心律失常作用。这项研究调查了LSG中Sema3a过表达是否通过减少心外和心脏内神经重塑而在MI后赋予抗心律失常作用。

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