Buzzi M G, Moskowitz M A
I Clinica Neurologica, Dipartimento di Scienze Neurologiche, Università degli Studi La Sapienza, Rome, Italy.
Pathol Biol (Paris). 1992 Apr;40(4):313-7.
Neurogenic inflammation has been proposed as a possible pathogenetic mechanism for migraine and cluster headache. Antidromic stimulation of trigeminal fibers causes plasma protein extravasation, mast cell activation and degranulation, vacuolation and increase in endothelial vesicle number within post capillary venules in rat dura mater. The antimigraine drugs sumatriptan and dihydroergotamine block the development of plasma extravasation and ultrastructural changes, as well as plasma calcitonin gene-related peptide (CGRP) increase in the superior sagittal sinus following electrical trigeminal ganglion stimulation. Sumatriptan and dihydroergotamine bind with high affinity to the 5-HT1D/1B receptors, thus suggesting that their neurogenic antiinflammatory activity is mediated by activation of 5-HT autoreceptors present on sensory fibers innervating blood vessels in dura mater.
神经源性炎症已被提出作为偏头痛和丛集性头痛可能的发病机制。对三叉神经纤维的逆向刺激会导致血浆蛋白外渗、肥大细胞活化和脱颗粒、空泡形成以及大鼠硬脑膜毛细血管后微静脉内内皮小泡数量增加。抗偏头痛药物舒马曲坦和双氢麦角胺可阻断电刺激三叉神经节后上矢状窦内血浆外渗和超微结构变化的发展，以及血浆降钙素基因相关肽（CGRP）的增加。舒马曲坦和双氢麦角胺与5-HT1D/1B受体具有高亲和力结合，因此表明它们的神经源性抗炎活性是由支配硬脑膜血管的感觉纤维上存在的5-HT自身受体激活介导的。
