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Paraventricular Nucleus (PVN) and Left stellate ganglion (LSG) are important central and peripheral components of cardiac sympathetic afferent reflex (CSAR) respectively. Studies have shown that endothelin-1 (ET-1) in PVN could increase sympathetic activity and elevated plasma level of ET-1 was related with ventricular arrhythmias (VAs). This study aimed to investigate whether ET-1 in LSG could increase cardiac sympathetic activity and thus facilitate post-infarction VAs in a canine model.
Twelve anesthetized open-chest male beagle dogs were randomly divided into the ET-1 group (n=6) and the control group (n=6). ET-1 (0.1ml, 0.1umol/ml) or saline (0.1ml) was microinjected into LSG separately. Ventricular effective refractory period (ERP), heart rate variability (HRV), LSG function and neural activity, serum norepinephrine (NE) level were measured at baseline and 30min after ET-1 injection. Then myocardial infarction (MI) was induced by ligating left anterior descending coronary artery. HRV, LSG neural activity and serum NE levels were measured 1h after MI. VAs occurred during the first hour after MI were recorded.
Compared to baseline, ET-1 microinjection significantly increased LSG function and neural activity and serum NE level, decreased HRV, shortened ventricular ERP, whereas, no significant changes of these indices were shown in the control group. MI induced a more significant decrease in HRV and increase in LSG neural activity and NE levels in the ET-1 group than those in the control group. The incidence of VAs was significantly higher in the ET-1 group than that in the control group.
ET-1 in LSG may increase the cardiac sympathetic activity and thus facilitate MI-induced VAs.