LL-VNS attenuates SK2 expression and incidence of arrhythmias following acute myocardial infarction in rats

Figures

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  FIGURE 1. The experimental protocol (A) and allocation to groups (B). AMI, acute myocardial infarction; BP, blood pressure; ERP, effective refractory period; HR, heart rate; HRV, heart rate variability; LL-VNS, low-level vagus nerve stimulation; LSG, left stellate ganglion.

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  FIGURE 2. Effects of LL-VNS on the electrophysiological properties of the ventricles. (A) Typical example of S1–S2 stimulation scheme in the measurement of ventricular ERP. (B) No significant differences among the three groups were observed at baseline. (C) LL-VNS prolonged ischemia-induced ERP measured at the ischemic area (IA). (D,E) No significant differences were observed among the three groups in ERP measured at the left or right non-ischemic area. (F) LL-VNS significantly reduced ischemia-induced ERP dispersion. (G) LL-VNS significantly mitigated ischemia-induced reduction in VFT. AMI, acute myocardial infarction; ERP, effective refractory period; IA, ischemic area; LL-VNS, low-level vagus nerve stimulation; NIA, non-ischemic area; VFT, ventricular fibrillation threshold. n = 15 per group. #P < 0.01 in a comparison with the Control group; *P < 0.01 in a comparison with the AMI group.

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  FIGURE 3. Effects of LL-VNS on neural activity in the left stellate ganglion (LSG). (A) Representative examples of LSG neural activity in the Control group, AMI group, and AMI + LL-VNS group. (B–E) Quantitative analysis of LSG neural activity in the three groups. LL-VNS significantly mitigated the AMI-induced increases in amplitude and frequency of LSG neural activity. AMI, acute myocardial infarction; LL-VNS, low-level vagus nerve stimulation. n = 15 per group. #P < 0.05 in a comparison with the Control group. *P < 0.05 in a comparison with the AMI group.

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  FIGURE 4. Effects of LL-VNS on cardiac autonomic nervous activity. Panels illustrate changes among the three groups between baseline and measurements taken 30 min after AMI in LF (A), HF (B), and LF/HF (C). AMI induced an increase in LF and LF/HF, but a reduction in HF, as indicated by comparison between the AMI and Control groups. In comparison with the AMI group, LF and LF/HF were significantly reduced in the LL-VNS group, but HF was increased. AMI, acute myocardial infarction; HF, high frequency; LF, low frequency; LF/HF, low frequency to high frequency ratio; LL-VNS, low-level vagus nerve stimulation. n = 15 per group. #P < 0.05 in a comparison with the Control group. *P < 0.05 in a comparison with the AMI group.

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  FIGURE 5. The occurrence of ventricular arrhythmias after complete occlusion of the left anterior descending branch. (A) ECG traces representing typical examples of VAs, including VPC, VT, and VF. (B) Comparison of the incidence of VPC throughout the entire 60 min between the AMI group and the AMI + LL-VNS group. (C) LL-VNS decreased the incidence of VT within 60 min after AMI. (D) LL-VNS shortened the duration of episodes of VT occurring within 60 min after AMI. (E) LL-VNS reduced the incidence of spontaneous VF. AMI, acute myocardial infarction; ECG, electrocardiogram; LL-VNS, low-level vagus nerve stimulation; VF, ventricular fibrillation; VPC, ventricular premature contraction. n = 15 per group. *P < 0.05 in a comparison with the AMI group.

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  FIGURE 6. Effects of low-level vagus nerve stimulation (LL-VNS) on SK expression induced by acute myocardial infarction (AMI). (A) Representative immunoblots of ventricular SK2. (B) Immunoblot analysis of ventricular SK2 protein expression. AMI contributed to a significant increase in ventricular SK2 protein expression; however, LL-VNS clearly reduced ventricular SK2 protein expression by comparison. (C) qRT-PCR analysis of ventricular SK2 mRNA expression. AMI induced an increase in SK2 mRNA expression; this was reduced in the LL-VNS group. n = 15 per group. #P < 0.05 in a comparison with the Control group. *P < 0.05 in a comparison with the AMI group.