Herbert M K, Tafler R, Schmidt R F, Weis K H
Institut für Anaesthesiologie, Universität Würzburg, Germany.
Agents Actions. 1993;38 Spec No:C25-7. doi: 10.1007/BF01991126.
Neurogenic inflammation is evoked by neuropeptides released from primary afferent terminals and, presumably, by other secondarily released inflammatory mediators. This study examines whether prostaglandins might participate in the development of neurogenic inflammation in humans and whether cyclooxygenase inhibitors have any anti-inflammatory effect on this type of inflammation. In healthy volunteers, neurogenic inflammation was elicited by epicutaneously applied capsaicin (1%), after systemic pretreatment with acetylsalicylic acid, or topically applied indomethacin compared to pretreatment with saline or vehicle, respectively. The extent of neurogenic inflammation was quantified by planimetry of visible flare size and recording the increase of superficial cutaneous blood flow (SCBF) with a laser Doppler flowmeter. Capsaicin-induced flare sizes and outside SCBF (both representing neurogenically evoked inflammation) were unaffected by acetylsalicylic acid or indomethacin. Only the capsaicin-induced increase of inside SCBF was attenuated by local pretreatment with indomethacin, reflecting the participation of prostaglandins in the inflammatory response of those areas which were in direct contact with capsaicin.
神经源性炎症由初级传入神经末梢释放的神经肽引发，可能还由其他继发释放的炎症介质引发。本研究探讨前列腺素是否可能参与人类神经源性炎症的发展，以及环氧化酶抑制剂对这类炎症是否具有抗炎作用。在健康志愿者中，与分别用生理盐水或赋形剂预处理相比，在全身用乙酰水杨酸预处理后，通过经皮应用辣椒素（1%）引发神经源性炎症，或者局部应用吲哚美辛引发神经源性炎症。通过对可见红晕大小进行平面测量以及用激光多普勒血流仪记录浅表皮肤血流（SCBF）的增加来量化神经源性炎症的程度。辣椒素诱导的红晕大小和外周SCBF（两者均代表神经源性诱发的炎症）不受乙酰水杨酸或吲哚美辛的影响。只有辣椒素诱导的内侧SCBF增加通过局部用吲哚美辛预处理而减弱，这反映了前列腺素参与了与辣椒素直接接触区域的炎症反应。
