Journal of The Showa Medical Association
Online ISSN : 2185-0976
Print ISSN : 0037-4342
ISSN-L : 0037-4342
EXPERIMENTAL RESEARCH OF ACUPUNCTURE EFFECT ON LOCAL MUSCLE PAIN
VI Effects of vasodilators and neuropeptide on recovery from the reduced twitch after tetanic stimulation
Jiro KUWAZAWAMichio SATOChifuyu TAKESHIGE
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JOURNAL FREE ACCESS

1987 Volume 47 Issue 1 Pages 81-88

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Abstract
It was supposed in our previous work that the relief of the muscle pain after needling to the muscle was induced by improvement of the reduced circulation in the pain producing muscle through axon reflex, since after denervation or treatment of capsaicin or atropine abolished this effect. In present experiment, this assumption was examined by the effects of vasodilators and of the neurotransmitters supposedly involved in primary afferent nerve associated with axon reflex on the model of pain producing muscle after tetanic stimulation. Tetanic 10Hz stimulation was applied for about 60 minutes to the gastrocnemius muscle of guinea pig anesthetized with nembutal. The reduced twitch height after tetanic stimulation was estimated as the pain produced state of the muscle. Needling was applied to the tetanized muscle and the recovery of twitch height from the reduced state was estimated as the index of needling effect. 250-400μ fine canula was inserted to the femoral artery toward the gastrocnemius muscle. Reduced twitch height after tetanic stimulation was recoverd more quickly by oblique needle insertion to the muscle than parallel insertion to the muscle fiber. Similar effect was produced by intraarterial injection of 0.3ml saline, lOng prostaglandin E2or 60μg isoproterenol. Less of these doses did not produce and higher doses did not further enchance the effect. Stimulation of the sciatic nerve to the muscle under treatment of d-tubocurarine produced similar effect to needling one and this effect was abolished by atropine. Both substance P (SP) and calcitonin generelated peptide (CGRP), produced similar effect. The effect of SP was not, but that of the CGRP was abolished by atropine. Relief of the muscle pain by needling to the muscle might be caused by the mechanism that needling stimulates the CGRP containing primary afferent nerve ending in the muscle and the excitation propagated to the axon-colaterales attached to the cholinergic nerve endings facilitating the release of acetylcholine to dilate the artery in the muscle.
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