Nitric oxide is not the sole determinant of hypercapnic or metabolically driven vasodilation in the cerebral...

Nitric oxide (NO) has recently been suggested to play a major role in a number of circulatory responses both within and outside the central nervous system. It has been linked to hypercapnic vasodilatation, metabolically driven changes in cerebral blood flow and hypoxia-induced changes in brain blood flow. In the studies the question of role of NO in hypercapnic vasodilatation and metabolically driven changes in flow is examined in the cat. Animals were anaesthetised with halothane and alpha-chloralose and ventilated. Cardiorespiratory parameters were monitored and kept within normal limits. Cerebral blood flow was monitored with laser Doppler flowmetry (CBFLDF) in the parietal cortex which metabolic activity was contemporaneously and continuously monitored using electrophysiological techniques. Hypercapnia was induced by increasing the end-expiratory CO2 to 8.1 +/- 0.4% and this produced a brisk rise in CBFLDF of 153 +/- 23%. Metabolic activity was increased by superfusion of the cortical surface with bicuculline (10 pmol) which increased cell firing and CBFLDF. Local administration of NG-nitro-L-arginine methyl ester (L-NAME) did affect the metabolically driven change in CBFLDF and only attenuated by 20% overall the hypercapnic vasodilator response. These studies suggest that at least in the anaesthetised cat NO does not play the pivotal role in these important vasodilator functions.