Role of ammonia as a buffer in the central nervous system

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During respiratory acidosis, increased brain buffering capacity and CSF bicarbonate concentration are associated with elevated CNS ammonia and glutamine and reduced glutamic acid content. To determine the exact buffering effects of ammonia in the brain and cerebrospinal fluid in the absence of any acid-base disturbance, anesthetized dogs, kept at a normal P a CO 2 , were given buffered NH 4Cl intravenously. Ammonia readily entered the CNS during infusion and despite a slight fall in arterial pH, CSF bicarbonate increased markedly and was linearly related to CSF ammonia. Brain ammonia initially rose but later declined as changes in the CNS concentration of glutamine and glutamic acid indicated activation of this pathway of ammonia detoxification. Despite nearly a ten-fold increase in brain lactate, intracellular pH was unchanged, as demonstrated by the stable brain CO 2 dissociation curve. These results indicate that ammonia can act as a strong buffer in the CNS to produce elevated CSF bicarbonate and a large intracellular base excess. Since the brain can regulate its ammonia content through the glutamine-glutamic acid pathway, CNS ammonia production is an important buffer mechanism for controlling the brain and CSF pH.