Carbon dioxide fixation in the brain.

Upon intracarotid administration of ammonia to cats, there is a significant increase of cerebral glutamine without a corresponding decrease in the level of cerebral glutamic acid (3). Similar observations in dogs have been reported by others (4). Since the supply of glutamic acid from the circulating blood is insufficient for the formation of the additional amount of glutamine, the dicarboxylic acid has to be synthesized in the brain.’ The continuous utilization of cr-ketoglutarate for this purpose would rapidly deplete the citric acid cycle of its intermediates unless they can be replenished by CO2 fixation. Therefore, the occurrence of significant COz fixation in brain in vivo was assumed (1, 2). Such an assumption seemed particularly justified, since carbon dioxide fixation had been demonstrated in the isolated retina 10 years ago (5), and the presence of the malic enzyme has also been shown in brain tissue (6). We wish to present experiments in which NaHC1403 was administered by intracarotid infusion to cats with and without ammonia; the results show a significant fixation of COz into amino acids by the cerebral cortex in z&o.