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去甲肾上腺素能机制在介导大鼠应激诱导的痛觉过敏中的作用

Noradrenergic mechanisms in mediation of stress-induced hyperalgesia in rats.

作者信息

Jørum Ellen

机构信息

Department of Physiology, University of Göteborg, GöteborgSweden.

出版信息

Pain. 1988 Mar;32(3):349-355. doi: 10.1016/0304-3959(88)90047-4.

Abstract

Exposure to a mild stressor (15 min of vibration) produced analgesia in some rats and hyperalgesia in other rats from the same batch treated in the same way. Rats which responded with decreased tail-flick latencies (TFL) showed signs of hyperemotionality during the stress procedure. Stress-induced hyperalgesia was abolished by the administration of diazepam (2.5 mg/kg i.p.) and clonidine (25 micrograms/kg i.p.). It is suggested that the reversal of hyperalgesia was due to the anxiolytic properties of the drugs. Yohimbine, an alpha 2-adrenoceptor antagonist (5 mg/kg i.p.), antagonized the effect of clonidine. The influence of clonidine on stress-induced hyperalgesia may be mediated by alpha 2-adrenoceptors.

摘要

暴露于轻度应激源(振动15分钟)会使同一批次以相同方式处理的一些大鼠产生镇痛作用,而另一些大鼠则产生痛觉过敏。尾部甩动潜伏期(TFL)缩短的大鼠在应激过程中表现出过度情绪化的迹象。地西泮(2.5毫克/千克腹腔注射)和可乐定(25微克/千克腹腔注射)可消除应激诱导的痛觉过敏。有人认为痛觉过敏的逆转是由于药物的抗焦虑特性。育亨宾,一种α2肾上腺素能受体拮抗剂(5毫克/千克腹腔注射),可拮抗可乐定的作用。可乐定对应激诱导的痛觉过敏的影响可能是由α2肾上腺素能受体介导的。

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