CALCITONIN GENE-RELATED PEPTIDE INCREASES BLOOD-FLOW AND POTENTIATES PLASMA-PROTEIN EXTRAVASATION IN THE RAT KNEE-JOINT
CALCITONIN GENE-RELATED PEPTIDE INCREASES BLOOD-FLOW AND POTENTIATES PLASMA-PROTEIN EXTRAVASATION IN THE RAT KNEE-JOINT
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DOI：
10.1111/j.1476-5381.1992.tb14404.x
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发表时间：
1992-07-01
影响因子：
7.3
通讯作者：
BRAIN, SD
中科院分区：
文献类型：
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作者：
CAMBRIDGE, H;BRAIN, SD
1测量降钙素基因相关肽（CGRP）和其他炎症的血管活性介质对戊巴比妥麻醉大鼠的滑膜血管中的血流量和血浆蛋白外渗到膝（股-胫）关节中的影响。2通过从滑膜腔清除氙-133来估计滑膜血流量的变化。CGRP（0.1 pmol和10 pmol）和前列腺素E1（PGE 1; 3 pmol和300 pmol）显着增加清除率从膝关节内注射后5分钟测量。P物质（10 pmol）对滑膜血流量没有影响。3用浓度高达0.1 mM的CGRP或浓度高达10 μ M的PGE 1对大鼠膝关节进行关节内灌注，通过静脉注射的I-125-灌注液中的白蛋白。4输注缓激肽显著增加了血浆外渗到膝关节（0.1 μ M）、5-羟色胺（1 μ M）和组胺（0.1 mM），与用台氏液灌注的相同动物的对侧关节相比，5用P物质灌注膝关节并不特异性诱导I-125，标记的白蛋白在滑膜腔中积累，即使在具有全身效应的剂量下，如通过显著的血浆外渗到其他组织中所观察到的。6组胺（0.1 mM）诱导的血浆外渗的增加通过与CGRP（0.1 μ M）和PGE 1（3 μ M）的共输注而增强。然而，与CGRP或PGE1.7共输注未增加对次最大剂量（0.1 μ M）缓激肽的反应，缓激肽诱导与组胺（0.1 mM）相似的血浆外渗。这些结果表明，CGRP是大鼠膝关节中有效的血管扩张剂。从感觉神经释放的CGRP可能与增加血管通透性的介质协同作用，以改变该部位的炎症反应。
1 The effects of calcitonin gene-related peptide (CGRP) and other vasoactive mediators of inflammation on blood flow in the synovial vessels and plasma protein extravasation into the knee (femoro-tibial) joint of the pentobarbitone-anaesthetized rat were measured.2 Changes in synovial blood flow were estimated by xenon-133 clearance from the synovial cavity. CGRP (0.1 pmol and 10 pmol) and prostaglandin E1 (PGE1; 3 pmol and 300 pmol) significantly increased clearance from the knee joint measured 5 min after intra-articular injection. Substance P (10 pmol) had no effect on synovial blood flow.3 Intra-articular perfusion of the rat knee with CGRP at concentrations up to 0.1 mM, or PGE1 at concentrations up to 10-mu-M, did not increase plasma extravasation into the synovial cavity measured by accumulation of intravenously injected I-125-albumin in the perfusate.4 Plasma extravasation into the knee was significantly increased by infusion of bradykinin (0.1-mu-M), 5-hydroxytryptamine (1-mu-M) and histamine (0.1 mM), compared with the contralateral joints in the same animals which were perfused with Tyrode solution.5 Perfusion of the knee joint with substance P did not specifically induce I-125-labelled albumin accumulation in the synovial cavity even at doses that had systemic effects as observed by marked plasma extravasation into other tissues.6 The increase in plasma extravasation induced by histamine (0.1 mM) was potentiated by co-infusion with CGRP (0.1-mu-M) and PGE1 (3-mu-M). However the response to a submaximal dose (0.1-mu-M) of bradykinin, which induced similar plasma extravasation to histamine (0.1 mM), was not increased by co-infusion with CGRP or PGE1.7 These results show that CGRP is a potent vasodilator in the rat knee. CGRP released from sensory nerves may act synergistically with mediators of increased vascular permeability to modify the inflammatory response in this site.