A BRIEF HYPOPERFUSION PRECEDES SPREADING DEPRESSION IF NITRIC-OXIDE SYNTHESIS IS INHIBITED

Spreading cortical depression (SCD) alters cerebral blood flow by mechanisms that are not well understood. To investigate the role of the likely endothelium-derived relaxing factor, nitric oxide, in the blood flow changes occurring during SCD in awake rats, nitric oxide synthesis was blocked using N(omega)-nitro-L-arginine methyl ester (L-NAME). During SCD there is an initial hyperperfusion followed by a longer-lasting hypoperfusion. Treatment with L-NAME, 30 mg/kg, reduced resting cerebral blood flow globally. During SCD, L-NAME treatment produced an additional brief phase of hypoperfusion which preceded the initial hyperperfusion. The magnitude of the initial hyperperfusion was less than expected. The subsequent longer-lasting hypoperfusion was unchanged. Nitric oxide plays an important role in the regulation of cerebral blood flow during SCD.