Towler P K, Brain S D
Pharmacology Group and Vascular Biology Research Centre, King's College London, UK.
Neurosci Lett. 1998 Nov 20;257(1):5-8. doi: 10.1016/s0304-3940(98)00770-8.
Stimulation of the saphenous nerve in the anaesthetised rat results in cutaneous neurogenic oedema formation. We have examined the effect of a tachykinin NK1 and a bradykinin B2 antagonist, and a mu-opioid agonist on plasma extravasation observed in response to two differing nerve stimulating parameters (10 V, 1 ms, 2 Hz and 25 V, 2 ms, 10 Hz). The NK1 antagonist SR140333 abolished oedema, supporting the theory that an NK1 agonist is a primary mediator of neurogenic oedema. The B2 antagonist HOE 140 had no effect, indicating a lack of involvement of B2 receptors in this response. The pre-junctionally acting mu-opioid agonist DAMGO significantly inhibited oedema formation at the 10 V, 1 ms, 2 Hz (P < 0.001), but not the 25 V, 2 ms, 10 Hz stimulation parameters. Thus a post-junctionally acting NK1 antagonist inhibited neurogenic oedema formation induced by both stimulation parameters, whilst a pre-junctionally acting mu-opioid agonist acted only at 10 V, 1 ms, 2 Hz parameters. These findings could be of interest with respect to therapeutic approaches of pathophysiological conditions which involve a neurogenic component.
在麻醉大鼠中刺激隐神经会导致皮肤神经源性水肿形成。我们研究了速激肽NK1拮抗剂、缓激肽B2拮抗剂和μ-阿片受体激动剂对在两种不同神经刺激参数（10伏、1毫秒、2赫兹和25伏、2毫秒、10赫兹）下观察到的血浆外渗的影响。NK1拮抗剂SR140333消除了水肿，支持了NK1激动剂是神经源性水肿主要介质的理论。B2拮抗剂HOE 140没有效果，表明B2受体未参与此反应。在10伏、1毫秒、2赫兹刺激参数下，突触前作用的μ-阿片受体激动剂DAMGO显著抑制水肿形成（P < 0.001），但在25伏、2毫秒、10赫兹刺激参数下则不然。因此，突触后作用的NK1拮抗剂抑制了由两种刺激参数诱导的神经源性水肿形成，而突触前作用的μ-阿片受体激动剂仅在10伏、1毫秒、2赫兹参数下起作用。这些发现可能与涉及神经源性成分的病理生理状况的治疗方法有关。
