Spasmogen release from an extracranial vascular bed evoked by neurohumoral stimuli and periods of vascular stasis.

The hypothesis that pro-inflammatory spasmogens may be generated locally in the vessels of the head by neurohumoral stimuli has been tested using an isolated extracranial vascular bed from the rabbit. No spasmogen release was detected after adenosine triphosphate, histamine, acetylcholine or noradrenaline and was seen rarely after tyramine and 5-hydroxytryptamine. Both sympathetic nerve stimulation and periods of vascular stasis released spasmogen, probably an E-type prostaglandin. The local generation of pro-inflammatory substances by excess sympathetic stimulation and/or vascular stasis might contribute to the development and maintenance of the acute migraine attack.