PGI2-INDUCED ACTIVATION AND SENSITIZATION OF ARTICULAR MECHANONOCICEPTORS
PGI2-INDUCED ACTIVATION AND SENSITIZATION OF ARTICULAR MECHANONOCICEPTORS
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DOI：
10.1016/0304-3940(91)90809-8
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发表时间：
1991-03-11
影响因子：
2.5
通讯作者：
GRUBB, BD
中科院分区：
文献类型：
--
作者：
BIRRELL, GJ;MCQUEEN, DS;GRUBB, BD
本文观察了前列腺素E_2（PGE_2）、前列腺素I_2（PGI_2）及其稳定的类似物cicaprost对麻醉大鼠踝关节机械感受器传入放电的影响。 动脉内注射PGI 2（0.01-0.1 μ g）或cicaprost（0.05-5 μ g）可引起对机械刺激的敏感性和大多数机械感受器的兴奋，而PGE 2（0.03-3 μ g）仅对少数伤害感受单位有微弱的作用。 这些结果表明，大鼠感觉传入神经上存在特异性PGI 2敏感受体（IP受体），并支持大鼠内源性PGI 2在降低炎症关节伤害性感受阈值中起重要作用的假设。
The effects of PGE2, PGI2 and the stable PGI2 analogue cicaprost on the afferent discharge of ankle joint mechanonociceptors were studied in the anaesthetized rat. Close-arterial injection of PGI2 (0.01-0.1-mu-g) or cicaprost (0.05-5-mu-g) caused both sensitization to mechanical stimulation and excitation of the majority of mechanonociceptors, whereas PGE2 (0.03-3-mu-g) had only weak effects on a small number of nociceptive units. These results suggest the existence of specific PGI2 sensitive receptors (IP receptors) on rat sensory afferent nerves, and support the hypothesis that in the rat endogenous PGI2 plays an important role in the lowering of nociceptive thresholds in inflamed joints.