Cardiac sympathetic afferent ablation to prevent ventricular arrhythmia complicating acute myocardial infarction by inhibiting activated astrocytes.

Enhanced cardiac sympathetic afferent reflex (CSAR) contributes to ventricular arrhythmia (VA) after acute myocardial infarction (AMI). However, central regulation mechanisms remain unknown. The aim of this study was to investigate whether local cardiac sympathetic afferent ablation (LCSAA) could reduce VA by inhibiting activated astrocytes in the hypothalamus paraventricular (PVN) in an AMI rat model. The rats were randomly divided into AMI, AMI + BD (baroreceptor denervation), AMI + LCSAA and AMI + BD+ LCSAA groups. Before the generation of AMI, BD and (or) LCSAA were performed. At 24 h after AMI, the incidence and duration of VA in AMI + LCSAA group and AMI + BD + LCSAA group were significantly reduced than AMI group (P < 0.05). Furthermore, LCSAA significantly reduced GFAP (a marker for activated astrocytes) positive cells and their projections as well as the level of TNF-α and IL-6 in the PVN of AMI + LCSAA group and AMI + BD+ LCSAA group, along with the decrease of neuronal activation in PVN and sympathetic nerve activity (P < 0.05). but BD had no obvious difference between AMI + LCSAA and AMI + BD + LCSAA group (P > 0.05). Therefore, LCSAA could decrease sympathoexcitation and VA occurrence in AMI rats by inhibiting astrocyte and neuronal activation in the PVN. Our study demonstrates that activated astrocytes may play an important role on CSAR in AMI.