结果：热痛觉过敏在肿瘤细胞植入后的12- 18天发生进展。
RESULTS: Thermal hyperalgesia developed between Days 12 and 18 after cancer cell inoculation.
各种因素引起的外周神经损伤可诱发痛觉过敏、感觉倒错等病理现象。
The peripheral nerve injury caused by some pathological factors results in pathological chronic pain, such as hyperalgesia, allodynia, and spontaneous pain ect.
因此，许多研究人员在寻求新的止痛药方时，都会把解除痛觉过敏及异位疼痛列入优先考量。
Many researchers, therefore, have amelioration of hyperalgesia and allodynia foremost in their minds as they hunt for new analgesics.
超前镇痛是通过防止外周和中枢敏化来降低伤害性刺激引起的痛觉过敏和痛觉异常的一种镇痛方法。
Preemptive analgesia is one of the analgesia measures which decreases the incidence of hyperalgesia and allodynia by reducing peripheral and central sensitization.
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和管理导致痛觉过敏，过敏热刺激和肌肉痛。
NGF levels are increased in inflammatory processes and administration of exogenous NGF leads to hyperalgesia, hypersensitivity to thermal stimulation and muscular pain.
背景：慢性痛包括痛觉过敏和痛觉感觉异常，是患者感到难以忍受和临床缺乏治疗手段的一种病理现象。
BACKGROUND: Chronic pain, including hyperalgesia and algesthesia paresthesia, is pathological phenomenons making the patients felt unendurable and lacking of clinical treatments.
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及神经病理性痛引发的热痛觉过敏。
The behavior results showed that blocking peripheral 5-HT_(2A)receptors inhibited the thermal hyperalgesia in inflammatory and neuropathic pain.
炎症时释放的许多炎症介质都能够与TRPV 1发生相互作用，产生疼痛或痛觉过敏，并且通过各种不同的信号通路来调制TRPV1的活性。
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.
炎症时释放的许多炎症介质都能够与TRPV 1发生相互作用，产生疼痛或痛觉过敏，并且通过各种不同的信号通路来调制TRPV1的活性。
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.
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