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缓慢传导的关节传入神经对缓激肽的反应性:实验性关节炎的影响

Responsiveness of slowly conducting articular afferents to bradykinin: effects of an experimental arthritis.

作者信息

Melinger Karl, Pawlak Matthias, Schepelmann Karsten, Schmidt Robert F

机构信息

Physiologisches Institut der Universität Würzburg, Röntgenring 9, D-97070 WürzburgGermany.

出版信息

Pain. 1994 Dec;59(3):335-343. doi: 10.1016/0304-3959(94)90019-1.

Abstract

Bradykinin (BK), an important inflammatory mediator and potent algogenic substance, is supposed to contribute to the generation of arthritic hyperalgesia and pain. The present study was undertaken to examine if an experimental kaolin/carrageenan arthritis sensitizes articular afferents to BK in the cat's knee joint using two different approaches. First, the proportion of afferent units activated by BK was assessed in fully inflamed joints and compared with corresponding data of normal knee joints. BK (injected i.a. as a bolus close to the joint) at the dose of 2.6 micrograms activated 60% of the units of groups II-IV in the inflamed state, compared to 71% in normal joints. The proportions of low- and high-threshold afferents activated by BK were similar, but more spontaneously active units than units without ongoing activity responded to BK both in inflamed and normal knee joints. Second, the responsiveness of individual afferent units to BK was examined during the development of inflammation. Units not activated by BK remained unresponsive after inflammation. From 11 units activated by BK, 3 units lost their responsiveness and in 4 other units the response to BK was reduced within 2-6 h after the onset of inflammation. Only in 4 units was the BK response increased in the inflamed joint. It is concluded that desensitizing rather than sensitizing processes are involved to change the response behavior of articular afferents to BK during acute experimental inflammation.

摘要

缓激肽(BK)是一种重要的炎症介质和强效致痛物质,被认为与关节炎性痛觉过敏和疼痛的产生有关。本研究采用两种不同方法,研究实验性高岭土/角叉菜胶性关节炎是否会使猫膝关节的关节传入神经对BK敏感。首先,评估在完全发炎的关节中被BK激活的传入神经单位的比例,并与正常膝关节的相应数据进行比较。剂量为2.6微克的BK(关节内注射大剂量)在发炎状态下激活了60%的II-IV组单位,而在正常关节中这一比例为71%。BK激活的低阈值和高阈值传入神经的比例相似,但在发炎和正常膝关节中,与无持续活动的单位相比,有更多自发活动的单位对BK有反应。其次,在炎症发展过程中检查单个传入神经单位对BK的反应性。未被BK激活的单位在炎症后仍无反应。在11个被BK激活的单位中,3个单位失去了反应性,另外4个单位在炎症发作后2-6小时内对BK的反应降低。只有4个单位在发炎关节中对BK的反应增加。得出的结论是,在急性实验性炎症期间,改变关节传入神经对BK反应行为的是脱敏而非致敏过程。

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