• Pain and hyperalgesia was caused by injury of tissue and peripheral nerves.

    组织损伤外周神经损伤后可导致过敏。

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  • RESULTS: Thermal hyperalgesia developed between Days 12 and 18 after cancer cell inoculation.

    结果痛觉过敏在肿瘤细胞植入12- 18发生进展。

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  • Conclusion There is a close relationship between epidural scar adhesion and thermal hyperalgesia.

    结论膜外瘢痕粘连重,则痛阈降低。热敏实验与硬膜外瘢痕粘连密切关系

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  • All these results suggested that VR1 is critical for the expression of inflammation-induced heat hyperalgesia.

    这些结果进一步说明VR1在炎症热痛敏的形成起着非常重要的作用。

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  • Many researchers, therefore, have amelioration of hyperalgesia and allodynia foremost in their minds as they hunt for new analgesics.

    因此许多研究人员寻求新的止痛药方时,都会把解除痛觉过敏异位疼痛列入优先考量。

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  • The behavior results showed that blocking peripheral 5-HT_(2A)receptors inhibited the thermal hyperalgesia in inflammatory and neuropathic pain.

    行为学结果显示阻断外周5-HT_(2A受体能够明显抑制慢性炎症神经病理性痛引发痛觉过敏

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  • Results Sprout number of DRG in experimental group rats decreased obviously and the symptom of hyperalgesia was improved as compared to control rats.

    结果实验组大鼠drg内交感明显减少,热痛过敏症状抑制。

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  • The peripheral nerve injury caused by some pathological factors results in pathological chronic pain, such as hyperalgesia, allodynia, and spontaneous pain ect.

    各种因素引起神经损伤可诱发痛觉过敏、感觉倒错等病理现象。

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  • Preemptive analgesia is one of the analgesia measures which decreases the incidence of hyperalgesia and allodynia by reducing peripheral and central sensitization.

    超前镇痛通过防止外周中枢敏化来降低伤害性刺激引起痛觉过敏和痛觉异常的种镇痛方法

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  • NGF levels are increased in inflammatory processes and administration of exogenous NGF leads to hyperalgesia, hypersensitivity to thermal stimulation and muscular pain.

    神经生长因子水平炎症过程中的神经生长因子增加外源性管理导致痛觉过敏过敏刺激肌肉

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  • Objective to investigate the role of peripheral N-methyl-D-aspartate (NMDA) receptors in the long-term hyperalgesia induced by peripheral injection of formalin in rats.

    目的观察n -甲基- D -天门冬氨酸(NMDA)受体对福尔·马林外注射所致时程痛敏的作用

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  • Many studies in recent years indicated that the activation and translocation of protein kinase C (PKC) of neurons in the dorsal horn of spinal cord was related with hyperalgesia.

    其详细机制并未完全阐明。近年研究表明脊髓后神经元蛋白激酶CPKC激活位移痛感觉及痛过敏的形成有关

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  • BACKGROUND: Chronic pain, including hyperalgesia and algesthesia paresthesia, is pathological phenomenons making the patients felt unendurable and lacking of clinical treatments.

    背景慢性包括痛觉过敏痛觉感觉异常,患者感到难以忍受临床缺乏治疗手段的一种病理现象

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  • In inflammatory pain, a number of inflammatory mediators are released, which modulate TRPV1 activity through various signal pathways or interact with TRPV1 generating pain or hyperalgesia.

    炎症释放许多炎症介质能够TRPV 1发生相互作用,产生疼痛痛觉过敏,并且通过各种不同信号通路来调制TRPV1活性

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  • AIM: to observe the changes of nitric oxide synthase NOS activity in the spinal cord posterior horn during carrageenan inflammatory pain and hyperalgesia, especially the time characteristics.

    目的观察菜胶炎性过敏脊髓后角一氧化氮合酶变化特别是时间特征。

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  • In clinic, pathological pain is one of the most frequently observed clinical symptoms, which is characterized by a persistent spontaneous pain, hyperalgesia and touch-evoked pain (allodynia).

    临床病理性表现持续性自发痛及伴有长时程持续性触诱发痛现象。

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  • Conclusion Intrathecal FC can reduce the mechanical and heat hyperalgesia in mice with bone cancer pain, and the astrocytes may play a role in the nociceptive transmission at the spinal level.

    结论鞘内注射氟代柠檬酸明显减轻骨癌小鼠机械痛敏,提示星形胶质细胞脊髓水平参与疼痛信息传递

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  • Conclusion Intrathecal FC can reduce the mechanical and heat hyperalgesia in mice with bone cancer pain, and the astrocytes may play a role in the nociceptive transmission at the spinal level.

    结论鞘内注射氟代柠檬酸明显减轻骨癌小鼠机械痛敏,提示星形胶质细胞脊髓水平参与疼痛信息传递

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