Anesthesia alters NO-mediated functional hyperemia

摘要: Abstract Many properties of nitric oxide, NO, (localization, diffusiveness, half-life, vasodilatory affects) have supported its potential role in mediating the link between local cerebral activity and blood flow. However, evidence that both supports refutes a for NO functional hyperemia been presented. The present study employed multiple oxide synthase inhibitors, two anesthetic regimes laser-Doppler flowmetry to test hypothesis is critically involved hyperemic response within rodent whisker-barrel cortex (WBC). In urethane anesthetized animals, responses were obtained before after 1 mg/kg atropine infusion, 30 i.v. l -NAME (N-Nitro- -arginine methylester) -NA -arginine) infusion or 25 7-NI (7-nitroindazole). was also tested group animals pretreated with halothane anesthesia. Neither magnitude flow nor time course altered by blockade administration when compared pre-infusion controls rats. contrast, exhibited 33% inhibition administration. Taken together, these data do not support primary rat WBC suggest previous reports may secondary anesthesia employed.