ROLE OF NITRIC-OXIDE IN REGULATING CEREBROCORTICAL OXYGEN-CONSUMPTION AND 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 oxygen consumption (CMRO(2)) and blood flow (CBF) to two levels of hypercapnia (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 using the Kety-Schmidt approach and CMRO(2) was calculated from the product of CBF and the arteriovenous (superior sagittal sinus) difference for oxygen. L-NAME treatment did not have a significant effect on either CMRO(2) or CBF under normocapnic conditions but inhibited the hypercapnic increase of CMRO(2) and the hypercapnic increase in CBF. These results suggest that NO plays a role in the response of CMRO(2) and CBF during hypercapnia and are consistent with the suggestion that at least part of the increase in CBF observed during hypercapnia is coupled to an increase in CMRO(2).