According to the trigeminovascular model of pain in migraine, sterile neuro
genic inflammation of dural vessels stimulates nociceptive fibres of the tr
igeminal nerve. Sumatriptan, a 5-HT1 receptor agonist, blocks this reaction
and mediates vasoconstriction of meningeal arteries. However, it is uncert
ain, whether sumatriptan also has a vasoconstrictive effect on cerebral art
eries, which may influence vasoneuronal coupling and induce secondary cereb
ral blood flow changes. We studied changes of cerebral blood flow velocity
(CBFV) and the pulsatility index (PI) in the posterior cerebral artery (PCA
) after stimulus activation before, 10 min and 30 min after subcutaneous ap
plication of 6 mg sumatriptan, in order to assess potential vasoactive effe
cts on cerebral circulation. CBFV was recorded from both PCAs simultaneousl
y in 27 migraineurs (twenty women, seven men, mean age 29 years), and arter
ial blood pressure (BP), heart rate (HR) and respiration rate (RR) were mon
itored. Although the mean diastolic blood pressure rose significantly from
75 mm Hg to 81 mm Hg (P<0.05) and systolic blood pressure and respiration r
ates remained constant, average CBFV values remained constant. Similarly, t
he relative increase of CBFV by visual stimulation, which is clearly higher
compared to controls in other studies (55.0% before, 52.6% after 10 min, a
nd 52.4% after 30 min), and absolute mean values for CBFV and PI did not ch
ange after visual stimulation. These results provide evidence against the h
ypothesis that sumatriptan produces vasoconstriction in the intracranial hu
man arterial circulation as a potential risk of cerebral ischemia. (C) 1999
Elsevier Science B.V. All rights reserved.