ROLE OF NITRIC-OXIDE IN REGULATING CEREBROCORTICAL OXYGEN-CONSUMPTIONAND BLOOD-FLOW DURING HYPERCAPNIA

The effect of the nitric oxide (NO) synthase inhibitor N-omega-nitro-L -arginine methyl ester (L-NAME) on the response of cerebrocortical oxy gen consumption (CMRO(2)) and blood flow (CBF) to two levels of hyperc apnia (P(a)co(2) similar to 60 mm Hg and P(a)co2 similar to 90 mm Hg) was investigated in ketamine-anesthetized rats. CBF was calculated usi ng the Kety-Schmidt approach and CMRO(2) was calculated from the produ ct of CBF and the arteriovenous (superior sagittal sinus) difference f or oxygen. L-NAME treatment did not have a significant effect on eithe r CMRO(2) or CBF under normocapnic conditions but inhibited the hyperc apnic increase of CMRO(2) and the hypercapnic increase in CBF. These r esults suggest that NO plays a role in the response of CMRO(2) and CBF during hypercapnia and are consistent with the suggestion that at lea st part of the increase in CBF observed during hypercapnia is coupled to an increase in CMRO(2).