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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >MUSCLE PAIN INDUCED BY STATIC CONTRACTION IN RATS IS MODULATED BY PERIPHERAL INFLAMMATORY MECHANISMS
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MUSCLE PAIN INDUCED BY STATIC CONTRACTION IN RATS IS MODULATED BY PERIPHERAL INFLAMMATORY MECHANISMS

机译:大鼠静态收缩诱导的肌肉疼痛通过外周炎症机制来调节

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Muscle pain is an important health issue and frequently related to static force exertion. The aim of this study is to evaluate whether peripheral inflammatory mechanisms are involved with static contraction-induced muscle pain in rats. To this end, we developed a model of muscle pain induced by static contraction performed by applying electrical pulses through electrodes inserted into muscle. We also evaluated the involvement of neutrophil migration, bradykinin, sympathetic amines and prostanoids. A single session of sustained static contraction of gastrocnemius muscle induced acute mechanical muscle hyperalgesia without affecting locomotor activity and with no evidence of structural damage in muscle tissue. Static contraction increased levels of creatine kinase but not lactate dehydrogenase, and induced neutrophil migration. Dexamethasone (glucocorticoid anti-inflammatory agent), DALBK (bradykinin B1 antagonist), Atenolol (beta 1 adrenoceptor antagonist), ICI 118,551 (beta 2 adrenoceptor antagonist), indomethacin (cyclooxygenase inhibitor), and fucoidan (non-specific selectin inhibitor) all reduced static contraction-induced muscle hyperalgesia; however, the bradykinin B2 antagonist, bradyzide, did not have an effect on static contraction-induced muscle hyperalgesia. Furthermore, an increased hyperalgesic response was observed when the selective bradykinin B1 agonist des-Arg(9)-bradykinin was injected into the previously stimulated muscle. Together, these findings demonstrate that static contraction induced mechanical muscle hyperalgesia in gastrocnemius muscle of rats is modulated through peripheral inflammatory mechanisms that are dependent on neutrophil migration, bradykinin, sympathetic amines and prostanoids. Considering the clinical relevance of muscle pain, we propose the present model of static contraction induced mechanical muscle hyperalgesia as a useful tool for the study of mechanisms underlying static contraction induced muscle pain. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.
机译:肌肉疼痛是一个重要的健康问题,经常与静力劳累有关。本研究的目的是评估外周炎症机制是否参与静态收缩诱导的大鼠肌肉疼痛。为此,我们开发了通过将电脉冲通过插入肌肉中的电极施加电极来执行的静电收缩诱导的肌肉疼痛模型。我们还评估了中性粒细胞迁移,Bradykinin,Sympath胺和前列醇的参与。胃肠杆菌肌肉持续静态收缩的单一会议诱导急性机械肌肉痛苦而不影响运动活动,没有肌肉组织中结构损伤的证据。静态收缩增加肌酸激酶但不是乳酸脱氢酶的水平,并诱导中性粒细胞迁移。地塞米松(糖皮质激素抗炎剂),DALBK(BRADYKININ B1拮抗剂),ATENOLOL(β1肾上腺素受体拮抗剂),ICI 118,551(β2肾上腺素受体拮抗剂),吲哚美辛(环氧氧酶抑制剂)和岩藻糖(非特异性选择蛋白抑制剂)都减少静态收缩诱导的肌肉痛觉;然而,Bradykinin B2拮抗剂Bradyzide没有对静态收缩诱导的肌肉痛觉的影响。 Furthermore, an increased hyperalgesic response was observed when the selective bradykinin B1 agonist des-Arg(9)-bradykinin was injected into the previously stimulated muscle.总之,这些发现证明,在大鼠中的腓肠肌静态收缩引起的机械痛觉过敏的肌肉通过依赖于中性粒细胞迁移,缓激肽,拟交感胺和前列腺素外周炎症机制调制。考虑到肌肉疼痛的临床相关性,我们提出了本发明的静态收缩诱导机械肌肉痛觉模型作为研究静态收缩诱导肌肉疼痛的机制的有用工具。 (c)2017年IBRO。 elsevier有限公司出版。保留所有权利。

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