Unidad de Investigación Médica en Inmunoquímica, Hospital de Especialidades del Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social (IMSS), Ciudad de México, Mexico.
Escuela Nacional de Medicina y Homeopatía, Instituto Politécnico Nacional, Ciudad de México, México.
Acupunct Med. 2020 Dec;38(6):388-395. doi: 10.1177/0964528420912251. Epub 2020 May 20.
Activation of the sympathetic nervous system attenuates inflammation via catecholamines. Recent evidence has shown that electroacupuncture (EA) activates neuronal networks involved in the release of dopamine and norepinephrine that control systemic inflammation. In muscle, catecholamines are related to cyclic adenosine monophosphate (cAMP). This signaling molecule has been implicated in recovery from sustained contractile activity, which may induce muscular pain, such as that which occurs during low back pain (LBP).
Our aim was to evaluate the effects of EA used for the control of LBP on the activation of the sympathetic nervous system in a randomized controlled clinical trial in athletes.
Two groups of athletes with acute or chronic low back pain were studied. EA, sham EA and pharmacological treatment (diclofenac sodium) were evaluated. The outcome measures included a pain score represented by a visual analogue scale (VAS) and serum levels of catecholamines quantified by enzyme-linked immunosorbent assay. In addition, blood was collected into chilled heparin tubes, placed in 96-well cell culture plates and incubated with an equal volume of Roswell Park Memorial Institute (RPMI) medium, with lipopolysaccharide (LPS) alone or with catecholamines. Tumor necrosis factor (TNF)-α levels in the supernatants were analyzed.
The results indicated that the initial pain ratings did not differ between the groups analyzed. EA induced epinephrine secretion but not norepinephrine or dopamine secretion. Although EA and pharmacological treatment did not differ in terms of pain relief, in vitro epinephrine and norepinephrine reduced TNF-α production in response to LPS stimuli.
EA activates the sympathetic nervous system and induces the release of epinephrine, which could ameliorate inflammation and protect muscular tissue in addition to relieving pain.
交感神经系统的激活通过儿茶酚胺来减轻炎症。最近的证据表明，电针（EA）激活了涉及多巴胺和去甲肾上腺素释放的神经元网络，这些神经递质控制着全身炎症。在肌肉中，儿茶酚胺与环磷酸腺苷（cAMP）有关。这种信号分子与从持续收缩活动中恢复有关，这种活动可能会引起肌肉疼痛，例如腰痛（LBP）时发生的疼痛。
我们的目的是在一项针对运动员的随机对照临床试验中评估 EA 用于控制 LBP 对交感神经系统激活的影响。
研究了两组患有急性或慢性腰痛的运动员。评估了 EA、假 EA 和药物治疗（双氯芬酸钠）。结局指标包括视觉模拟评分（VAS）表示的疼痛评分和通过酶联免疫吸附试验定量的儿茶酚胺血清水平。此外，将血液收集到冷肝素管中，放入 96 孔细胞培养板中，并与等体积的罗格斯大学纪念医院（RPMI）培养基孵育，单独使用脂多糖（LPS）或与儿茶酚胺一起孵育。分析上清液中肿瘤坏死因子（TNF）-α的水平。
结果表明，分析的各组之间初始疼痛评分没有差异。EA 诱导肾上腺素分泌，但不诱导去甲肾上腺素或多巴胺分泌。尽管 EA 和药物治疗在缓解疼痛方面没有差异，但体外肾上腺素和去甲肾上腺素可减少 LPS 刺激引起的 TNF-α产生。
EA 激活交感神经系统并诱导肾上腺素释放，除了缓解疼痛外，还可以减轻炎症并保护肌肉组织。
