Role of nitric oxide and ATP-sensitive K+ channels in regulation of basal blood flow and hypercapnic vasodilatation of cerebral blood vessels in rabbit

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

Role of local nerves and prostaglandins in regulation of basal blood flow and hypercapnic vasodilatation of cerebral blood vessels in the rabbit

The mechanisms underlying cerebral vasodilatation during hypercapnia are not fully understood. To examine the role of nerves and prostaglandins in the regulation of basal blood flow and in hypercapnia-induced vasodilatation in the cerebral blood vessels of rabbit. Cerebral blood flow was measured by laser Doppler flowmeter in 18 NZW rabbits anesthetized with sodium pentobarbital. Tetrodetoxin was administered locally and indomethacin [a prostaglandin inhibitor] both locally and systemically before and during induction of hypercapnia. Basal cerebral blood flow did not change significantly in response to local tetrodetoxin, and also after local and systemic administration of indomethacin. Hypercapnia increased cerebral blood flow by 25.9 +/- 3.9% before and by 24.3 +/- 6.5% after administration of TTX and by 22.1 +/- 7.1% before and by 18.2 +/- 6.3% after administration of indomethacin. In the rabbit, prostaglandin and regional nerves had no role in regulation of basal cerebral blood flow, nor did they contribute to cerebral vascular dilatation during hypercapnia