Low-level tragus stimulation improves autoantibody-induced hyperadrenergic postural tachycardia syndrome in rabbits.
Low-level tragus stimulation improves autoantibody-induced hyperadrenergic postural tachycardia syndrome in rabbits.
复制标题
低水平耳屏刺激可改善兔自身抗体诱导的高肾上腺素能体位性心动过速综合征。
DOI：
10.1016/j.hroo.2022.12.001
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发表时间：
2023-02
期刊：
影响因子：
--
通讯作者：
Yu, Xichun
中科院分区：
文献类型：
--
作者：
Guo, Yankai;Li, Hongliang;Deng, Jielin;Zhang, Gege;Fischer, Hayley;Stavrakis, Stavros;Yu, Xichun
关键词：
最近的研究表明抗肾上腺素能自身抗体参与体位性体位性心动过速综合征（POTS）的病理生理过程。本研究的目的是验证经皮低水平耳屏刺激（LLTS）改善兔自身免疫性POTS模型中自身抗体诱导的自主神经功能障碍和炎症的假设。用α1-肾上腺素能受体肽和β1-肾上腺素能受体肽共同免疫6只新西兰大白兔，产生拟交感神经抗体。在免疫前、免疫后6周和免疫后10周分别对意识清醒的家兔进行倾斜试验，每天给予4周的LLTS治疗。每只兔子都作为自己的对照。在没有明显血压变化的情况下，在免疫兔子中观察到体位心率增加，证实了我们之前的报道。倾斜试验期间心率变异性的功率谱分析显示，免疫兔的交感神经活动优于副交感神经活动，表现为低频功率显著增加，高频功率显著降低，低高频比显著增加。免疫兔血清炎症因子也显著升高。LLTS抑制体位性心动过速，改善交感迷走神经平衡，增加乙酰胆碱分泌，降低炎症细胞因子表达。体外实验证实了抗体的产生和活性，在这项短期研究中没有发现LLTS对抗体的抑制作用。在兔自身抗体诱导的高肾上腺素能性POTS模型中，LLTS可改善心脏自主神经失衡和炎症，提示LLTS可作为一种新的神经调节治疗方法。
Recent studies have demonstrated that antiadrenergic autoantibodies are involved in the pathophysiology of postural orthostatic tachycardia syndrome (POTS). The purpose of this study was to test the hypothesis that transcutaneous low-level tragus stimulation (LLTS) ameliorates autoantibody-induced autonomic dysfunction and inflammation in a rabbit model of autoimmune POTS. Six New Zealand white rabbits were co-immunized with peptides from the α1-adrenergic and β1-adrenergic receptors to produce sympathomimetic antibodies. The tilt test was performed on conscious rabbits before immunization, 6 weeks after immunization, and 10 weeks after immunization with 4-week daily LLTS treatment. Each rabbit served as its own control. An enhanced postural heart rate increase in the absence of significant change in blood pressure was observed in immunized rabbits, confirming our previous report. Power spectral analysis of heart rate variability during the tilt test showed a predominance of sympathetic over parasympathetic activity in immunized rabbits as reflected by markedly increased low-frequency power, decreased high-frequency power, and increased low-to-high-frequency ratio. Serum inflammatory cytokines were also significantly increased in immunized rabbits. LLTS suppressed the postural tachycardia, improved the sympathovagal balance with increased acetylcholine secretion, and attenuated the inflammatory cytokine expression. Antibody production and activity were confirmed with in vitro assays, and no antibody suppression by LLTS was found in this short-term study. LLTS improves cardiac autonomic imbalance and inflammation in a rabbit model of autoantibody-induced hyperadrenergic POTS, suggesting that LLTS may be used as a novel neuromodulation therapy for POTS.
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