This project is directed at the evaluation of nitric oxide (NO) as a potential mediator of the coupling of local cerebral blood flow to local cerebral metabolic and/or functional activities. The Laboratory is using its standard [14C]iodoantipyrine and [14C]deoxyglucose methods for measuring local cerebral blood flow and glucose utilization, respectively, to examine the changes in local blood flow associated with experimentally induced changes in local functional and metabolic activities before and after administration of N G-monomethyl-L-arginine, an inhibitor of the enzyme that synthesizes nitric oxide. The results thus far have shown that CO2, a product of energy metabolism and a popular candidate for the role of the putative mediator, does not dilate cerebral vessels via NO mechanisms.
