Summary: The effect of the nitric oxide (NO) synthase inhibitor Nw-nitro-L-arginine methyl ester (L-NAME) on the response of cerebrocortical oxygen consumption (CMR02) and blood flow (CBF) to two levels of hyper capnia (PaC02 -60 mm Hg and Pac02 -90 mm Hg) was investigated in ketamine-anesthetized rats. CBF was cal culated using the Kety-Schmidt approach and CMR02 was calculated from the product of CBF and the arterio venous (superior sagittal sinus) difference for oxygen. L-NAME treatment did not have a significant effect onThe mechanism by which hypercapnia exerts its effect on cerebral blood flow is elusive. While part of the increase in cerebral blood flow is mediated through a local vascular reaction to hypercapnic ac idosis (Kontos et aI., 1977;Busija and Heistad, 1984), a number of central neuronal and peripheral neurohormonal factors may also play a role (Shalit et aI., 1967; MacKenzie et aI., 1976; Hemmingsen et aI., 1979; Berntman et aI., 1979; Siesjo et aI., 1980; Reddy et aI., 1986;Bryan, 1990; Dora et aI., 1992).Nitric oxide (NO) is a recently discovered mes senger molecule that mediates a wide variety of physiological and pathological effects in the cardio vascular, endocrinological, peripheral nervous, and central nervous systems (for reviews see Moncada et aI., 1991;Ignarro, 1991;and Synder, 1992). NO is 503either CMR02 or CBE under normocapnic conditions but inhibited the hypercapnic increase of CMR02 and the hy percapnic increase in CBF. These results suggest that NO plays a role in the response of CMR02 and CBF during hypercapnia and are consistent with the suggestion that at least part of the increase in CBF observed during hyper capnia is coupled to an increase in CMR02•

No abstract