Anesthesia alters NO-mediated functional hyperemia

Many properties of nitric oxide. NO. (localization, diffusiveness. half-lif e, vasodilatory affects) have supported its potential role in mediating the link between local cerebral activity and blood Row. However. evidence that both supports and refutes a role for NO in functional hyperemia have been presented. The present study employed multiple nitric oxide synthase inhibi tors, two anesthetic regimes and laser-Doppler flowmetry to test the hypoth esis that NO is critically involved in mediating the functional hyperemic r esponse within rodent whisker-barrel cortex (WBC). In urethane anesthetized animals, functional hyperemic responses were obtained both before and afte r 1 mg/kg atropine infusion, 30 mg/kg i.v. L-NAME (N-Nitro-L-arginine methy lester) infusion, 30 mg/kg L-NA (N-Nitro-L-arginine) infusion or 25 mg/kg 7 -NI (7-nitroindazole). L-NAME was also tested in a group of animals pretrea ted with halothane before urethane anesthesia. Neither the magnitude of the blood flow response nor its time course was altered by NO blockade or atro pine administration when compared to pre-infusion controls in urethane anes thetized rats. In contrast. animals that were pretreated with halothane exh ibited a 33% inhibition of functional hyperemia after L-NAME administration . Taken together, these data do not support a primary role for NO in rat WB C functional hyperemia and suggest that previous reports of inhibition may have been secondary to the anesthesia employed. (C) 2001 Elsevier Science B .V. All rights reserved.