Comparisons of pain relief mechanisms between needling to the muscle, static magnetic field, external qigong and needling to the acupuncture point.

Author: Ryu H//Lee HS//Shin YS//Chung SM//Lee MS//Kim HM//Chung HT
Conference/Journal: Acupunct Electrotherapeutics Res, Intl J
Date published: 1996
Other: Volume ID: 24 , Issue ID: 2 , Pages: 119-31 , Special Notes: In English , Word Count: 414

Pain relief mechanisms of needling to the pain-producing muscle, application of a static magnetic field or external qigong, and needling to the acupuncture point were investigated in an experimentally designed pain producing muscle of animals. Single isometric twitch height in situ was reduced gradually by 10 Hz tetanic stimulation for one hour of the gastrocnemius muscle of guinea pigs. This reduction of twitch height was recovered by injection of 0.3-1 ml saline to the artery of this muscle, or of injection of a vasodilator, isoproterenol dissolved in 0.1 ml saline. Hence, reduction of twitch h recovery of it could be induced be recovery of circulation. Since it is easily considered that a pain substance might be accumulated in a muscle under reduced circulation, and such an accumulated substance might be eliminated by recovery of circulation, the reduction of twitch height after tetanic stimulation could be estimated as the pain-producing muscle and recovery of twitch, as the pain relieving muscle. 1) Needling to the pain muscle, 2) application of a static magnetic field or external qigong to the muscle, and 3) needling to the acupuncture point recovered the reduced twitch height due to tetanic stimulation. Atropine abolished this effect induced by the above 1, 2 and 3 procedures. Hence, the cholinergic vasodilator nerve might be involved in the induction of this effect. A sciatic nerve cut did not influence the effect of 1), but abolished the effect of 3). Denervation and capsaicin abolished the effect of 1). Substance P and a calcitonin gene- related
peptide (CGRP) recovered the reduced twitch height, and atropine blocked the effect of CGRP, but did not block that of substance P. The effect of 2) was equivalent to that of anticholinesterase. A rostral lesion of the contralateral anterior hypothalamus did not abolish the effect of 3, but a caudal lesion of this region did. Electrical stimulation of this region produced an effect similar to that of 3). From these results, it was concluded that muscle pain relief by these procedures might be induced by recovery of circulation due to the enhanced release of acetylcholine as a result of activation of the cholinergic vasodilator nerve endings innervated to the muscle artery. However, manners of activation of the cholinergic nerve was different in effects of 1), 2) and 3). 1) might be induced by axon reflex of the CGRP nerve, 2) might be induced by inhibition of cholinesterase and
3) might be induced by a somato-autonomic reflex. The reflex center of this might be in the anterior hypothalamus.
Department of Microbiology and Immunology, Wonkwang University School of Medicine, Chonbuk, Republic of Korea