Manning D C, Raja S N, Meyer R A, Campbell J N
Department of Anesthesiology, Johns Hopkins University, Baltimore, MD.
Clin Pharmacol Ther. 1991 Dec;50(6):721-9. doi: 10.1038/clpt.1991.212.
Pain and hyperalgesia, the perceptual campanions of tissue injury and inflammation, are thought to be in part attributable to the sensitization of primary afferent nociceptors by endogenously released chemicals, such as bradykinin. Bradykinin (0.1 to 10 nmol in 10 microliters) evoked a dose-dependent pain, hyperalgesia to heat stimuli, and wheal and flare when injected in a double-blind manner into the volar forearm intradermally. Though hyperalgesia to mechanical stimuli is a conspicuous feature of inflammatory pain, none was measurable for any of the bradykinin doses in response to graded nylon monofilament probes. A second injection of bradykinin (5- or 30-minute intervals) at the same site produced markedly less pain and hyperalgesia to heat stimuli, indicating that the algesic and hyperalgesic effects of bradykinin undergo tachyphylaxis. These findings suggest that bradykinin alone cannot account for all aspects of the hyperalgesia that occurs after inflammation.
疼痛和痛觉过敏是组织损伤和炎症的感知伴发症状，部分原因被认为是内源性释放的化学物质（如缓激肽）使初级传入伤害感受器致敏所致。以双盲方式将缓激肽（10微升中含0.1至10纳摩尔）皮内注射到掌侧前臂时，会引起剂量依赖性疼痛、对热刺激的痛觉过敏以及风团和潮红。虽然对机械刺激的痛觉过敏是炎性疼痛的一个显著特征，但对于任何剂量的缓激肽，用分级尼龙单丝探针检测时均未测得对机械刺激的痛觉过敏。在同一部位再次注射缓激肽（间隔5或30分钟）时，引起的疼痛和对热刺激的痛觉过敏明显减轻，这表明缓激肽的致痛和痛觉过敏作用会发生快速耐受。这些发现表明，仅缓激肽不能解释炎症后发生的痛觉过敏的所有方面。
