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Sodium 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. Five 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 (VMCA), and diameters of the superficial temporal artery (STA) and radial artery (RA). All 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 (PetCO2). We found that SNP decreased the velocity of the VMCA, but this was canceled by a decrease of cerebral blood flow (CBF) due to hypocapnia. The 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.


Song Guo, Messoud Ashina, Jes Olesen, Steffen Birk. The effect of sodium nitroprusside on cerebral hemodynamics and headache in healthy subjects. Cephalalgia : an international journal of headache. 2013 Apr;33(5):301-7

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PMID: 23405018

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