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Previous studies demonstrated that increased inflammation was associated with the incidence and severity of ventricular arrhythmias (VAs) and left stellate ganglion (LSG) hyperactivity promotes VAs. The present study aimed to investigate whether exogenous recombinant IL-1β could aggravate VAs through increasing the activity of the LSG.
Eighteen canines were averagely and randomly divided into IL-1β group and saline group. A final volume of 0.1ml IL-1β (5μg/ml) or saline was microinjected into the LSG. Ventricular effective refractory period (ERP), action potential duration (APD), LSG function defined as the relative change of maximal systolic blood pressure (SBP) in response to direct LSG electrical stimulation (20Hz, 0.1 ms pulse width), and LSG neural activity were measured at baseline, 10 min after the injection and 60 min after acute ischemia. Acute ischemia was induced through occlusion of left anterior descending branch (LAD) and VAs were recorded for 60 min. The LSG tissue samples were collected to evaluate the expression of NGF and c-fos.
Ventricular ERP and APD90 were significantly decreased by IL-1β when compared with saline group. Also, increased LSG function and LSG spontaneous neuron activity were observed in IL-1β group under normal condition. More importantly, increased LSG neural activity induced by ischemia in the saline group was further aggravated by IL-1β and VAs were significantly increased in the IL-1β group. The expression of NGF and c-fos, which promoting the pathological neural remodeling of LSG, was up-regulated by IL-1β.
IL-1β aggravates VAs induced by acute ischemia, possibly through the over-activation of the LSG.