C. Kruuse et al., Dipyridamole dilates large cerebral arteries concomitant to headache induction in healthy subjects, J CEREBR B, 20(9), 2000, pp. 1372-1379
Dipyridamole is used for secondary prophylaxis in ischemic stroke and as a
vasodilator agent in myocardial scintigraphy. An important side effect to a
dministering dipyridamole is headache. The aim of the current study was to
investigate the effects of dipyridamole on cerebral blood flow, large arter
y diameter, and headache induction. Twelve healthy subjects were included i
n this single-blind placebo-controlled study in which placebo (0.9% NaCl) a
nd dipyridamole 0.142 mg/kg.min were administered intravenously over 4 minu
tes 1 hour apart. Blood flow velocity in the middle cerebral artery (V-mca)
was recorded by transcranial Doppler and regional cerebral blood flow in t
he middle cerebral artery (rCBF(mcu)) was measured using single photon emis
sion computed tomography and (133)Xenon-inhalation. Blood pressure, heart r
ate, and pCO(2) were measured repeatedly. Headache response was scored ever
y 10 minutes on a verbal scale from 0 to 10 (10 = worst). Dipyridamole caus
ed a decrease in pCO(2) (P < 0.001). pCO(2) corrected rCBF(mca) was 11.7 +/
- 6.9 mL/100 g min after placebo versus 31.2 +/- 6.9 after dipyridamole (P
greater than or equal to 0.05). pCO(2) corrected V-mca decreased 8.4% +/- 1
1.7 (P < 0.001) after dipyridamole, indicating a mean 5.6% +/- 6.7 (P = 0.0
05) relative increase of the arterial diameter. After dipyridamole the medi
an peak headache score was 2 (range 0 to 7) compared with 0 (range 0 to 3)
after placebo (P = 0,02). Dilatation of the middle cerebral artery outlaste
d the headache response. In conclusion, dipyridamole causes a modest pCO(2)
independent dilatation of the MCA, which is time-linked to the onset, but
not to the cessation, of headache.