Abstract
The effect of acute hypocapnia upon the energy state of the brain tissue, exposed to sustained hyperammonemia, was evaluated in lightly anesthetized rats. The acute hypocapnia was associated with a mostly unaffected energy state of the frontal lobe. In the cerebellum and the brainstem there were inconsistent changes in the adenylates, indicating a more labile energy homeostasis, despite significantly lower ammonia contents compared with the cerebrum. The metabolism of α-ketoglutarate is discussed as a possible mediating mechanism for the toxicity of ammonia.