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.
Department of Neurology, University of Connecticut Health Center, Farmington 06030-1845.
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Duckrow
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000378:metabolism / Q000494:pharmacology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D013181:Cortical Spreading Depression / Q000502:physiology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000378:metabolism* / Q000502:physiology; D010296:Parietal Lobe / Q000033:anatomy & histology / Q000098:blood supply; D051381:Rats; D017207:Rats, Sprague-Dawley
D009569:Nitric Oxide; D001120:Arginine; D019331:NG-Nitroarginine Methyl Ester