Absence of vasoactive peptide release from brain to cerebral circulation during onset of XXXX .

@entity1 @entity2795 @entity10133 @entity7766 @entity16 @entity10132 @entity2704 @entity10
In eight @entity1 carotid angiography was required for evaluation of transient @entity16 . Cerebral blood flow results, angiography and clinical observations subsequently suggested the diagnosis of @entity2704 . We measured plasma concentrations of substance @entity10133 ), neuropeptide Y ( @entity7766 ), calcitonin gene-related peptide ( @entity10132 ) and vasoactive intestinal peptide (VIP) in repeated blood samples obtained from the carotid artery and the internal jugular vein in conjunction with cerebral angiography followed by 4 to 6 repeated recordings of regional cerebral blood flow (rCBF) with the intracarotid Xenon-133 injection technique. This technique is known to induce attacks of @entity2795 in many sufferers. Four @entity1 developed aura symptoms. In three this was succeeded by throbbing @entity10 . Typical, @entity2704 -related, focal hypoperfusion occurred in conjunction with the aura symptoms. The remaining four @entity1 had no symptoms or rCBF changes. There were no systematic or statistically significant changes over time in arterial-venous plasma concentrations or in the release rates of any of the peptides. All migraineurs had an overall elevated mean @entity10132 value compared to control values from the literature. The overall plasma levels of the potent vasoconstrictor @entity7766 were higher (p < 0.10) in the group that developed symptoms and rCBF changes (136 pmol/l) than in the non-symptomatic group (97 pmol/l). The difference in @entity7766 levels could perhaps be associated with the focal rCBF decrease seen in the attack group.
