Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Cardiothoracic Surgery, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, China.
Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Heart Rhythm. 2019 Aug;16(8):1251-1260. doi: 10.1016/j.hrthm.2019.02.027. Epub 2019 Feb 25.
High output subcutaneous nerve stimulation (ScNS) remodels the stellate ganglia and suppresses cardiac arrhythmia.
The purpose of this study was to test the hypothesis that long duration low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of paroxysmal atrial tachycardia (PAT) in ambulatory dogs.
We prospectively randomized 22 dogs (11 males and 11 females) into 5 different output groups for 2 months of ScNS: 0 mA (sham) (n = 6), 0.25 mA (n = 4), 1.5 mA (n = 4), 2.5 mA (n = 4), and 3.5 mA (n = 4).
As compared with baseline, the changes in the durations of PAT episodes per 48 hours were significantly different among different groups (sham, -5.0 ± 9.5 seconds; 0.25 mA, 95.5 ± 71.0 seconds; 1.5 mA, -99.3 ± 39.6 seconds; 2.5 mA, -155.3 ± 87.8 seconds; and 3.5 mA, -76.3 ± 44.8 seconds; P < .001). The 3.5 mA group had a greater reduction in sinus heart rate than did the sham group (-29.8 ± 15.0 beats/min vs -14.5 ± 3.0 beats/min; P = .038). Immunohistochemical studies showed that the 0.25 mA group had a significantly increased while 2.5 mA and 3.5 mA stimulation had significantly reduced growth-associated protein 43 nerve densities in both atria and ventricles. The plasma norepinephrine concentrations in the 0.25 mA group was 5063.0 ± 4366.0 pg/mL, which was significantly higher than that in the other groups of dogs (739.3 ± 946.3; P = .009). There were no significant differences in the effects of simulation between males and females.
In ambulatory dogs, low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of PAT episodes while high output ScNS is antiarrhythmic.
高输出皮下神经刺激(ScNS)重塑星状神经节并抑制心律失常。
本研究旨在验证以下假设,即长时间低输出 ScNS 会导致心脏神经发芽,并增加去甲肾上腺素浓度和间歇性心房性心动过速(PAT)的持续时间。
我们前瞻性地将 22 只狗(11 只雄性和 11 只雌性)随机分为 5 个不同的 ScNS 输出组,进行 2 个月的治疗:0 mA(假)(n = 6)、0.25 mA(n = 4)、1.5 mA(n = 4)、2.5 mA(n = 4)和 3.5 mA(n = 4)。
与基线相比,不同组间 48 小时内 PAT 发作持续时间的变化差异有统计学意义(假,-5.0 ± 9.5 秒;0.25 mA,95.5 ± 71.0 秒;1.5 mA,-99.3 ± 39.6 秒;2.5 mA,-155.3 ± 87.8 秒;3.5 mA,-76.3 ± 44.8 秒;P<0.001)。3.5 mA 组窦性心率降低幅度大于假刺激组(-29.8 ± 15.0 次/分 vs -14.5 ± 3.0 次/分;P =.038)。免疫组化研究表明,0.25 mA 组心房和心室的生长相关蛋白 43 神经密度明显增加,而 2.5 mA 和 3.5 mA 刺激则明显减少。0.25 mA 组的血浆去甲肾上腺素浓度为 5063.0 ± 4366.0 pg/mL,明显高于其他组(739.3 ± 946.3;P =.009)。在雄性和雌性动物中,刺激的效果没有显著差异。
在活动的狗中,低输出 ScNS 导致心脏神经发芽,增加血浆去甲肾上腺素浓度和 PAT 发作持续时间,而高输出 ScNS 则具有抗心律失常作用。