Hughes G S, Lichstein P R, Whitlock D, Harker C
Phys Ther. 1984 Jul;64(7):1062-6. doi: 10.1093/ptj/64.7.1062.
A study of 31 healthy volunteers was done to test the hypothesis that analgesia produced by low frequency/high intensity (LoF/Hil) transcutaneous electrical nerve stimulation (TENS) is mediated by release of beta-endorphin (beta-E). After randomization, Group 1 (n = 10) received no stimulation (placebo); Group 2 (n = 9) received 30 minutes of high frequency/low intensity (HiF/Lol) TENS; and Group 3 (n = 12) received 30 minutes of low frequency/high density (LoF/Hil) TENS. Blood pressure, pulse, plasma beta-E levels, and evoked potential response were measured before and after treatment. Mean plasma beta-E increased with treatment in Groups 2 and 3 and fell in Group 1, but the difference between the groups was not statistically significant. Sixty-seven percent of Groups 2 and 3 showed an increase in plasma beta-E levels compared with 30 percent in Group 1 (two-sample test of proportions, p less than .05). Evoked potential response, a measure of pain threshold, varied directly with plasma beta-E level independent of the type of treatment applied. This study did not demonstrate a difference between the effects of HiF/Lol versus Lof/Hil TENS on plasma beta-E in healthy subjects.
对31名健康志愿者进行了一项研究，以检验低频/高强度（LoF/Hil）经皮电神经刺激（TENS）产生镇痛作用是由β-内啡肽（β-E）释放介导的这一假设。随机分组后，第1组（n = 10）不接受刺激（安慰剂）；第2组（n = 9）接受30分钟的高频/低强度（HiF/Lol）TENS；第3组（n = 12）接受30分钟的低频/高密度（LoF/Hil）TENS。在治疗前后测量血压、脉搏、血浆β-E水平和诱发电位反应。第2组和第3组的平均血浆β-E随治疗增加，第1组下降，但组间差异无统计学意义。第2组和第3组中有67%的受试者血浆β-E水平升高，而第1组为30%（比例的双样本检验，p<0.05）。诱发电位反应作为疼痛阈值的一项指标，与血浆β-E水平直接相关，与所应用的治疗类型无关。本研究未证明高频/低强度与低频/高密度TENS对健康受试者血浆β-E的影响存在差异。
