Brain carbonic anhydrase activity in rats in experimental hepatogenic encephalopathy.

Carbonic anhydrase (CA) activity was measured in the brains of rats subjected to repeated administration of thioacetamide (TAA), known to produce symptoms of hepatogenic encephalopathy (HE). In the early phase of the experiment, an increase of the enzyme activity was observed, which correlated well with elevated blood ammonia, while the brain ammonia remained unchanged. Prolonged TAA treatment resulted in the cessation of the activation of CA coinciding with the increase of brain ammonia above control levels. The results, in addition to supporting the idea that CA participates in ammonia detoxication in brain, may also indicate that the enhancement of the enzyme activity represents an adaptation mechanism to the increased ammonia load during HE.