Abstract
It was clinically reported that the acupuncture needling is effective to relieve muscle pain originated from spasm of muscle. Such acupuncture needling effect might be attributed to the improvement of the reduced circulation in spastic state of the muscle since it was clinically reported that reduced temperature of the spastic muscle was recovered to normal by acupuncture needling. The reduced circulation might accumulate and release the pain substances in ischemic state and under these condition, the ischemic pain was produced by muscular movement. Improvement of the circulation should exclude the pain substances in the ischemic state.
This concept was proved by the experimental model of the ischemic pain of the muscle. The isometric twitch height of the guinea pig gastrocnemius in situ was gradually reduced to about half of the control by 10 Hz tetanic stimulation of the muscle for 60 minutes. This state of the reduced twitch was estimated as that to produce the ischemic pain. Oblique needle insertion into the tetanized muscle just after tetanic stimulation facilitated recovery from the reduced twitch height and almost completely restored it taking about 2 hours. Recovery of twitch height should be attributed to recovery of reduced circulation. The accumulated pain substances might be excluded by recovering the reduced circulation. This needling effect disappeared after denervation, atropine or capsaicine treatment. Therefore, the axon reflex and the cholinergic vasodilator nerve to the blood vessel in the muscle might be involved in producing this needling effect. Intra-arterial injection of saline and vasodilator produced similar effect to that of needling in tetanized muscle. Stimulation of the sciatic nerve under treatment of d-tubocurarine also produced similar effect to that of the needling. This effect was abolished by atropine. Intra-arterial injection of the transmitter of primary afferent nerve which was depleted by capsaicine such as substance P or calcitonin-gene-related peptide (CGRP) produced similar effect to that of needling. The effect of substance P was not, but that of CGRP was blocked by atropine. Therefore, needle insertion stimulates the CGRP containing primary afferent nerve endings. The axon colaterals of this nerve endings innervates to the nerve endings of the cholinergic vasodilator nerve in the sympathetic nerve. The release of acetylcholine from the cholinergic nerve to dilate the blood vessle is facilitated by needle insertion through these connection of the nerve endings.
Recovery of the reduced twitch of the gastrocnemius muscle after tetanic stimulation was induced by another procedure, needle insertion to the ipsilateral L4-S1 perivertebral muscle. Insertion of the needle to the skin of the area had no effect on twitch height. This needling effect was abolished by the cutting of the sciatic nerve, caudal lesion with knife cut of the anterior hypothalamus or intra-venous injection of 0.1 mg/kg atropine. The rostral lesion with knife cut of the anterior hypothalamus did not influence on this effect. Focal electrical stimulation of the restricted region in the anterior hypothalamus just above the optic chiasma produced similar effect to that of needling to the contralateral perivertebral muscle.
Potential was evoked from the stimulating electrodes inserted to the anterior hypothalamus by stimulation through the inserted needle to the contralateral perivertebral muscle which caused acupuncture effect. Therefore, this acupuncture needling effect was produced by somato-autonomic reflex.
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