Alpha-Phenyl N-tert-butyl nitrone (PBN) increases the cortical cerebral blood flow by inhibiting the breakdown of nitric oxide in anesthetized rats.

Abstract

The effects of intravenous administration of alpha-phenyl N-tert-butyl nitrone (PBN) on cortical cerebral blood flow (CBF) were examined in Wistar rats under pentobarbital anesthesia and artificial ventilation. The cortical CBF in parietal cortex was measured by laser Doppler flowmetry. Intravenous administrations of 2 mg/kg and 20 mg/kg of PBN dose-dependently produced significant increases in cortical CBF and decreases in systemic blood pressure (BP). To examine whether these increased responses in cortical CBF produced by PBN were associated with the vasodilatation system of nitric oxide (NO), the NO synthase inhibitor L-NG-nitroarginine (L-NOArg), which is an analog of L-arginine, was used to inhibit the NO-related-vasodilatative system. Since the PBN-induced responses in the cortical CBF were much attenuated in L-NOArg-treated rats (30 mg/kg, i.v.), it was inferred that NO-related vasodilatation was strongly associated with the PBN-induced increase in cortical CBF.