Author + information
- Yuhong Wang,
- Lilei Yu and
- Bing Huang HongJiang
Previous studies have shown that the leptin, a peptide hormone produced by adipose tissue, could activate the sympathetic nervous system which has been shown to contribute to the pathogenesis of ischemia-induced ventricular arrhythmias (VAs). However, the role of leptin in cardiac sympathetic ganglion, especially the left stellate ganglion (LSG), is unclear. The aim of this study was to investigate the role of leptin in LSG activation, and its effect on ischemia-induced VAs.
16 pentobarbital anesthetized dogs were included. 0.1ml of saline
(control group, n=8) or leptin (30μg/ml) (leptin group, n=8) was microinjected into LSG, respectively. At baseline and 30min after the administration, the LSG function defined as blood pressure increases in response to LSG stimulation (20Hz, 0.1ms pulse duration, 7.5V) were measured, and the LSG neural activity was also recorded. Then, acute ischemia model was induced by left anterior descending occlusion (LADO). Ventricular arrhythmia and the LSG neural activity were continuously measured for 1 hour.
At baseline state, there were no significant differences between the control group and the leptin group in the function and neural activity of LSG. 30min after administration, leptin significantly increased LSG function[(31±4)% vs (51±4)%, P0.05] and LSG neural activity [Frequency: (40±3) impulses/min vs (77±3) impulses /min; Amplitude:(0.03±0.01)mV vs (0.10±0.01)mV; P0.05 for both] when compared with the control group. Moreover, during 1 hour of acute ischemia, the leptin group was associated with higher LSG neural activity [Frequency : (106±4) impulses/min vs (148±3) impulses /min; Amplitude: (0.13±0.01)mV vs (0.21±0.01)mV; P0.05 for both] and increased incidence of ventricular arrhythmias [ventricular premature beat numbers: (79±2) vs (125±2); ventricular tachycardia numbers: (12±1) vs (22±1); ventricular tachycardia duration: (16.7±0.9)s vs (37.7±2.4)s; P0.05 for all] compared with the control group.
Leptin could increase the LSG neural activity, and thereby promoting acute ischemia-induced VAs.