RESUMEN
The mechanisms underlying cerebral hypercapnic vasodilatation are not fully understood. To investigate the role of nitric oxide [NO] and ATPsensitive potassium [KATP] channels in basal blood flow regulation and hypercapnia-induced vasodilatation in rabbit cerebral blood vessels. The change in cerebral blood flow was measured by a laser Doppler flowmeter in 18 New Zealand white rabbits, in two groups, under general anesthesia with sodium pentobarbital. Nomega- nitro-L-arginine methyl ester [L-NAME] and glibenclamide were administered locally and systemically before and during induction of hypercapnia. The change in cerebral blood flow was not significant following local and systemic L-NAME administration, showing a nonsignificant role of local and systemic NO in regulation of rabbit basal cerebral blood flow. Hypercapnia increased cerebral blood flow by 17.3 +/- 4.4% before and 17.3 +/- 5.8% after local, and 5.8 +/- 3.2% [p<0.05] after systemic L-NAME administration. The change in cerebral blood flow was not significant after local and systemic administration of glibenclamide indicating a lack of KATP channel role in basal blood flow regulation. Hypercapnia increased cerebral blood flow by 27.2 +/- 8.7% before and 24.7 +/- 6.4% after local, and 49.3 +/- 9.7% after systemic administration of glibenclamide [p: NS in both cases]. Regional NO production had no role in basal cortical blood flow regulation and systemic NO contributed to 66% increment in cerebral blood flow during hypercapnia. Also, the KATP channels did not mediate the effect of NO or other vasodilators responsible for increasing cerebral blood flow during hypercapnia