The effect of sodium nitroprusside on cerebral hemodynamics and headache in healthy subjects
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The effect of sodium nitroprusside on cerebral hemodynamics and headache in healthy subjects. / Guo, Song; Ashina, Messoud; Olesen, Jes; Birk, Steffen.
I: Cephalalgia, 2013.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - The effect of sodium nitroprusside on cerebral hemodynamics and headache in healthy subjects
AU - Guo, Song
AU - Ashina, Messoud
AU - Olesen, Jes
AU - Birk, Steffen
PY - 2013
Y1 - 2013
N2 - InvestigationSodium nitroprusside (SNP) is a powerful vasodilatory agent that, similarly to glyceryl trinitrate (GTN), releases nitric oxide (NO) but in contrast does not pass the blood-brain barrier. Nevertheless, it has already been used in animal models without any knowledge of its headache-inducing potential. We hypothesized that SNP would induce headache and vasodilation of cephalic and radial but not cerebral arteries.MethodsFive healthy volunteers received intravenous infusions of SNP in a non-randomized dose-titration (1-5 µg/kg/min) study. We recorded headache intensity (verbal rating scale from 0 to 10), velocity in the middle cerebral artery (V(MCA)), and diameters of the superficial temporal artery (STA) and radial artery (RA).ResultsAll participants reported a dose-related headache (median peak = 2.5, range 0-3). SNP dilated the STA and RA, caused a marked increase of heart rate and a decrease of mean arterial pressure (MAP) and partial pressure of end-tidal carbon dioxide (P(et)CO(2)). We found that SNP decreased the velocity of the V(MCA), but this was canceled by a decrease of cerebral blood flow (CBF) due to hypocapnia.ConclusionThe present study shows that SNP is a headache-inducing agent with close similarities to headaches induced by GTN and probably without effect on intracerebral arteries.
AB - InvestigationSodium nitroprusside (SNP) is a powerful vasodilatory agent that, similarly to glyceryl trinitrate (GTN), releases nitric oxide (NO) but in contrast does not pass the blood-brain barrier. Nevertheless, it has already been used in animal models without any knowledge of its headache-inducing potential. We hypothesized that SNP would induce headache and vasodilation of cephalic and radial but not cerebral arteries.MethodsFive healthy volunteers received intravenous infusions of SNP in a non-randomized dose-titration (1-5 µg/kg/min) study. We recorded headache intensity (verbal rating scale from 0 to 10), velocity in the middle cerebral artery (V(MCA)), and diameters of the superficial temporal artery (STA) and radial artery (RA).ResultsAll participants reported a dose-related headache (median peak = 2.5, range 0-3). SNP dilated the STA and RA, caused a marked increase of heart rate and a decrease of mean arterial pressure (MAP) and partial pressure of end-tidal carbon dioxide (P(et)CO(2)). We found that SNP decreased the velocity of the V(MCA), but this was canceled by a decrease of cerebral blood flow (CBF) due to hypocapnia.ConclusionThe present study shows that SNP is a headache-inducing agent with close similarities to headaches induced by GTN and probably without effect on intracerebral arteries.
U2 - 10.1177/0333102412475239
DO - 10.1177/0333102412475239
M3 - Journal article
C2 - 23405018
JO - Cephalalgia
JF - Cephalalgia
SN - 0800-1952
ER -
ID: 48419636