Iversen H K, Olesen J
Department of Neurology, Glostrup Hospital, University of Copenhagen, Denmark.
Cephalalgia. 1994 Dec;14(6):437-42. doi: 10.1046/j.1468-2982.1994.1406437.x.
The molecular mechanisms of migraine pain have not yet been clarified. Monoamine and the peptide neurotransmitters involved in neurogenic inflammation do not cause significant head pain. Our previous studies of glyceryl trinitrate (GTN) and histamine-induced headaches have suggested that nitric oxide (NO) is the causative molecule in migraine pain. We furthermore suggest that substances capable of inducing experimental vascular headache do so via a common mediator which is NO. Finally, it is suggested that drugs exert their antimigraine activity by inhibiting NO or subsequent steps in the cascade of intracellular reactions triggered by NO. These novel observations change current views on vascular headache mechanisms and the importance of NO as an initiator of the migraine attacks dictates new approaches to the pharmacological treatment of migraine and other vascular headaches.
偏头痛疼痛的分子机制尚未阐明。参与神经源性炎症的单胺和肽类神经递质不会引起明显的头痛。我们之前对硝酸甘油（GTN）和组胺诱发头痛的研究表明，一氧化氮（NO）是偏头痛疼痛的致病分子。我们进一步认为，能够诱发实验性血管性头痛的物质是通过一种共同的介质即NO来实现的。最后，有人提出药物通过抑制NO或由NO触发的细胞内反应级联中的后续步骤来发挥其抗偏头痛活性。这些新的观察结果改变了目前对血管性头痛机制的看法，并且NO作为偏头痛发作启动因子的重要性决定了偏头痛和其他血管性头痛药物治疗的新方法。
