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Increased intramuscular concentration of bradykinin increases the static fusimotor drive to muscle spindles in neck muscles of the cat.

作者信息

Pedersen J, Sjölander P, Wenngren B I, Johansson H

机构信息

Department of Work Physiology and Technology, National Institute for Working Life, Umeå Sweden.

出版信息

Pain. 1997 Mar;70(1):83-91. doi: 10.1016/s0304-3959(96)03305-2.

Abstract

The aim of the present study was to investigate if increased intramuscular concentrations of bradykinin (BK) in one muscle influence the activity in primary and secondary muscle spindle afferents (MSAs) originating from both ipsi- and contralateral muscles, via fusimotor reflexes. The ipsilateral trapezius (TR) and the splenius (SP) muscles were subjected to sinusoidal stretches and 2-3 MSAs were simultaneously recorded from these muscles. Responses of 29 MSAs (15 SP and 14 TR) were registered in five adult cats anaesthetised with alpha-chloralose. Intramuscular injections of 0.5 ml BK (6-86 micrograms/ml) were administered to both the ipsi- and contralateral SP and TR muscles. Similar doses of BK (5-10 micrograms) have been shown to induce muscle pain when injected into the temporal muscle in man. The responsiveness of the MSAs to the injections of BK was 86% and 87.5% from the contralateral TR and SP muscles, respectively. The effects were predominantly static onto the MSAs. The duration of the effects was on average 3.5-4 min, however some effects lasted for more than 15 min. The effects were always abolished after cutting the nerve to the injected muscle. The large majority of the spindle afferents were unresponsive to i.m. Tyrode injections (23 of 29). For the afferents that were responsive to injection of Tyrode, the effects were always considerably smaller and with shorter duration than those evoked by BK injections. Thus, increased intramuscular concentrations of BK may excite primary and secondary MSAs from ipsi- and contralateral muscles, via fusimotor reflexes evoked most probably by activity in chemosensitive muscle afferents. The results are discussed in relation to a recent hypothesis on pathophysiological mechanisms behind genesis, spread and perpetuation of muscle tension and pain in chronic musculoskeletal pain syndromes.

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