Vidal C, Jacob J J
Life Sci. 1982;31(12-13):1241-4. doi: 10.1016/0024-3205(82)90352-6.
Emotional, non-noxious stress consisting of inescapable holding or exposure to novelty were found to produce clearcut and reproducible hyperalgesia in the rat. The mechanisms of the two stress hyperalgesia appeared to be different: 1) hypophysectomy enhanced holding hyperalgesia but reduced novelty hyperalgesia, indicating that pituitary factors respectively compensate (through opioids ?) and participate (through ACTH ?) in stress hyperalgesia; 2) diazepam did not alter holding hyperalgesia but abolished novelty hyperalgesia. The two types of stress hyperalgesia might represent animal models of anxiogenic hyperalgesia observed in human: as for clinical anxieties, they are alleviated or not by diazepam.
研究发现，由无法逃避的束缚或接触新事物所构成的情绪性、非伤害性应激会在大鼠身上产生明确且可重复的痛觉过敏。这两种应激性痛觉过敏的机制似乎有所不同：1）垂体切除增强了束缚性痛觉过敏，但减弱了新事物诱导的痛觉过敏，这表明垂体因子分别通过阿片类物质（？）进行代偿以及通过促肾上腺皮质激素（？）参与应激性痛觉过敏；2）地西泮不会改变束缚性痛觉过敏，但会消除新事物诱导的痛觉过敏。这两种类型的应激性痛觉过敏可能代表了在人类身上观察到的焦虑性痛觉过敏的动物模型：就像临床焦虑症一样，它们会被地西泮缓解或无缓解。
