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首页> 外文期刊>Pain. >Increased intramuscular concentration of bradykinin increases the static fusimotor drive to muscle spindles in neck muscles of the cat.
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Increased intramuscular concentration of bradykinin increases the static fusimotor drive to muscle spindles in neck muscles of the cat.

机译:缓激肽的肌肉内浓度增加会增加对猫颈部肌肉中的纺锤体的静态融合运动驱动力。

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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.
机译:本研究的目的是研究肌内缓激肽(BK)浓度的增加是否通过融合运动反射影响源自同侧和对侧肌肉的原发性和继发性肌梭传入神经(MSA)的活动。对同侧斜方肌(TR)和脾脏(SP)进行正弦拉伸,同时从这些肌肉中记录2-3个MSA。在五只用α-氯醛麻醉的成年猫中记录了29种MSA(15 SP和14 TR)的反应。对同侧和对侧SP和TR肌肉均进行0.5 ml BK(6-86微克/ ml)的肌内注射。已显示类似剂量的BK(5-10微克)在注入人的颞肌时会引起肌肉疼痛。对侧TR和SP肌肉的MSA对BK注射的反应分别为86%和87.5%。影响对MSA而言主要是静态的。效果持续时间平均为3.5-4分钟,但是某些效果持续超过15分钟。在切断神经到注射的肌肉后,这种作用总是被消除。绝大多数纺锤传入对肌无力。蒂罗德针剂(29中的23)。对于对Tyrode注射有反应的传入神经,其效果总是比BK注射引起的效果小得多,持续时间更短。因此,增加的肌内BK浓度可能通过化学敏感的肌肉传入活动引起的融合运动反射,激发同侧和对侧肌肉的初级和次级MSA。讨论了有关慢性肌肉骨骼疼痛综合征的发生,肌肉张力和疼痛的起源,扩散和永存背后的病理生理机制的最新假说的结果。

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