Pertovaara Antti, Kemppainen Pentti, Johansson Gunnar, Karonen Sirkka-Liisa
Department of Physiology, University of Helsinki, Siltavuorenpenger 20 J, 00170 Helsinki 17, Finland Department of Clinical Chemistry, University of Helsinki, Meilahti Hospital, 00290 Helsinki 29 Finland.
Pain. 1982 Aug;13(4):379-384. doi: 10.1016/0304-3959(82)90006-9.
The dental pain threshold elevation produced by non-painful, low-frequency transcutaneous electrical nerve stimulation (TENS) in healthy humans was not reduced by the administration of 0.8 mg of naloxone i.v. Neither ACTH, prolactin nor growth hormone (GH) release were related to the pain threshold elevations. The present study indicates that the dental pain threshold elevation during non-painful, low-frequency TENS is not based on the same opioid-dependent mechanisms as the dental pain threshold elevation during acupuncture or the clinical analgesia during low-frequency TENS. Stress or other adenohypophyseal mechanisms involving ACTH, prolactin or GH do not explain the analgesia induced by non-painful, low-frequency TENS.
在健康人体中，非疼痛性低频经皮电神经刺激（TENS）所产生的牙痛阈值升高，不会因静脉注射0.8毫克纳洛酮而降低。促肾上腺皮质激素（ACTH）、催乳素和生长激素（GH）的释放均与疼痛阈值升高无关。本研究表明，非疼痛性低频TENS期间的牙痛阈值升高，其依据的阿片类物质依赖机制与针刺期间的牙痛阈值升高或低频TENS期间的临床镇痛所依据的机制不同。涉及ACTH、催乳素或GH的应激或其他腺垂体机制，无法解释非疼痛性低频TENS所诱导的镇痛作用。
