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急性关节炎症——机制与介质

Acute joint inflammation--mechanisms and mediators.

作者信息

Scott D T, Lam F Y, Ferrell W R

机构信息

Institute of Physiology, University of Glasgow, Scotland.

出版信息

Gen Pharmacol. 1994 Nov;25(7):1285-96. doi: 10.1016/0306-3623(94)90151-1.

DOI:10.1016/0306-3623(94)90151-1
PMID:7896038
Abstract
  1. This review discusses factors contributing to acute joint inflammation, particularly sensory neuropeptides. 2. Mediators known to contribute importantly to the inflammatory process include cytokines, eicosanoids, complement and the kinin systems, histamine and 5-hydroxytryptamine and sensory neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP). 3. The pro-inflammatory neurokinins, SP and CGRP, are present in nerves innervating joints and could significantly contribute to the increased vascular permeability and hyperaemia occurring in acute arthritis. 4. Although perhaps contributing to the pathogenesis of chronic inflammatory joint disease, there is little evidence for involvement of the sympathetic nervous system in acute models of inflammation.
摘要
  1. 本综述讨论了导致急性关节炎症的因素,特别是感觉神经肽。2. 已知对炎症过程有重要作用的介质包括细胞因子、类二十烷酸、补体和激肽系统、组胺、5-羟色胺以及感觉神经肽P物质(SP)和降钙素基因相关肽(CGRP)。3. 促炎神经激肽SP和CGRP存在于支配关节的神经中,可能在急性关节炎中导致血管通透性增加和充血。4. 虽然交感神经系统可能参与慢性炎症性关节疾病的发病机制,但在急性炎症模型中几乎没有证据表明其参与其中。

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Acute joint inflammation--mechanisms and mediators.急性关节炎症——机制与介质
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Distribution of substance P and calcitonin gene related peptide immunoreactivity in the normal feline knee.P物质和降钙素基因相关肽免疫反应性在正常猫膝关节中的分布
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