Role of Nitric Oxide in Regulating Cerebrocortical Oxygen Consumption and Blood Flow during Hypercapnia

Abstract

The effect of the nitric oxide (NO) synthase inhibitor N_ω-nitro-l-arginine methyl ester (l-NAME) on the response of cerebrocortical oxygen consumption (CMRO₂) and blood flow (CBF) to two levels of hypercapnia (P_aco₂ ∼ 60 mm Hg and P_aco₂ ∼ 90 mm Hg) was investigated in ketamine-anesthetized rats. CBF was calculated using the Kety–Schmidt approach and CMRO₂ 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 CMRO₂ or CBE under normocapnic conditions but inhibited the hypercapnic increase of CMRO₂ and the hypercapnic increase in CBF. These results suggest that NO plays a role in the response of CMRO₂ 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 CMRO₂.