Investigation: 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.
Methods: 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).
Results: 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.
Conclusion: 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.