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DOI 10.1111/1755-5922.12437

Медицинская библиотека · Cardiovascular therapeutics · 2018

Chronic median nerve modulation reduces ventricular arrhythmia and improves ventricular function in a postmyocardial infarction rabbit model.

Zhai Zhengqin, Zhao Shuang, Tang Min, Jia Liujun, Zhang Shu

СтатьяПеревод пока не подготовлен

Аннотация

AIM: Median nerve stimulation (MNS) is a novel neuromodulation approach for treatment of ventricular arrhythmia, but little is known about its chronic effects. The aim of this study was to investigate the effects of chronic MNS on ventricular arrhythmia and ventricular dysfunction postmyocardial infarction (MI).

METHOD: Two weeks after MI, 12 rabbits were randomly divided into control and MNS groups, and chronic MNS was performed in MNS group for 2 weeks. Ventricular function and arrhythmias; sympathetic innervation and activity; and interleukin-1 β (IL-1 β) and norepinephrine (NE) levels were analyzed.

RESULTS

Both the total number of premature ventricular complex and episodes of ventricular tachycardia were lower in MNS group than in control group (20 560 ± 10 314 beats vs 70 079 ± 37 184 beats, P = .021, and 115 ± 63 episodes vs 307 ± 164 episodes, P = .034, respectively). Compared with control group, MNS decreased the cardiac sympathetic nerve density and level of circulating NE in MNS group (1798.42 ± 644.07 μm2 /mm2 vs 1003.79 ± 453.00 μm2 /mm2, P = .041, and 20.86 ± 4.54 pg/mL vs 11.07 ± 1.43 pg/mL, P = .002, respectively). MNS also improved the left ventricular ejection fraction (59.07 ± 1.91% vs 49.77 ± 3.47%, P = .003) and inhibited the level of IL-1 β in serum (69.19 ± 4.71 pg/mL vs 85.93 ± 12.80 pg/mL, P = .013).

CONCLUSION

Chronic MNS appears to protect against ventricular arrhythmia and improves ventricular function post-MI, which may be mediated by suppressing cardiac sympathetic activity and anti-inflammatory effects.

Для цитирования: Zhai Zhengqin, Zhao Shuang, Tang Min, Jia Liujun, Zhang Shu. Chronic median nerve modulation reduces ventricular arrhythmia and improves ventricular function in a postmyocardial infarction rabbit model.. Cardiovascular therapeutics. 2018. DOI: 10.1111/1755-5922.12437.

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