Role of kinins in pain and hyperalgesia: psychophysical studies in a patient with kininogen deficiency.
Role of kinins in pain and hyperalgesia: psychophysical studies in a patient with kininogen deficiency.
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激肽在疼痛和痛觉过敏中的作用：激肽原缺乏患者的心理物理学研究。
DOI：
10.1042/cs0830337
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Colman,RW
中科院分区：
文献类型：
--
作者：
Raja,SN;Campbell,JN;Meyer,RA;Colman,RW
1. 缓激肽被认为是与损伤和炎症相关的疼痛和痛觉过敏的重要介质。我们对一名完全激肽原缺乏的患者进行了心理物理研究，以确定缓激肽缺乏是否与疼痛敏感性异常有关。热刺激大鱼际隆起引起的疼痛在局部烧伤之前和之后进行了测试，这已被证明在正常受试者中引起痛觉过敏。此外，研究了前臂皮内注射缓激肽（0.1 ~ 10 μg）引起的疼痛，以及缓激肽对热刺激引起的疼痛的影响。患者将所有热刺激引起的疼痛强度与3°45°C刺激引起的疼痛强度进行评分。患者无毛皮肤的热痛阈值（45°C）与年龄匹配的对照受试者相似（n= 5），与先前在年轻对照受试者中观察到的相似。烧伤导致疼痛阈值降低和阈以上刺激引起的疼痛增加。痛觉过敏的程度在年龄匹配的对照组和较年轻的对照组中观察到的范围内。因此，激肽对于热损伤后痛觉过敏的发生并不是必需的。在对照组中，皮内注射缓激肽对热刺激产生疼痛和痛觉过敏。在患者中，皮内注射缓激肽引起的疼痛很小，对热刺激没有痛觉过敏。因此，先天性激肽原的缺乏可能与缓激肽受体的缺乏有关。
1. Bradykinin is considered to be an important mediator of pain and hyperalgesia associated with injury and inflammation. Psychophysical studies were conducted in a patient with complete kininogen deficiency to determine whether the absence of bradykinin was associated with abnormalities in pain sensibility. Pain evoked by heat stimuli to the thenar eminence was tested before and after a localized burn, which has been shown to cause hyperalgesia in normal subjects. In addition, pain evoked by intradermal administration of bradykinin (0.1–10 μg) to the forearm and the effects of bradykinin on pain induced by heat stimuli were studied. The patient rated the intensity of pain evoked by all heat stimuli relative to the pain induced by a 3s 45°C stimulus.2. The patient's heat pain threshold (45°C) in the glabrous skin was similar to that of age-matched control subjects (n= 5) and to that previously observed in younger control subjects.3. The burn resulted in a decrease in pain threshold and an increase in pain induced by suprathreshold stimuli. The magnitude of hyperalgesia was within the range observed in the age-matched control subjects and in younger control subjects. Thus, kinins are not essential for the development of hyperalgesia after heat injury.4. In control subjects, intradermal injections of bradykinin produced pain and hyperalgesia to heat stimuli. In the patient, intradermal bradykinin injections induced minimal pain and no hyperalgesia to heat stimuli. Thus, congenital absence of kininogens may be associated with a deficiency in bradykinin receptors.