Abstract
The rates of accession of sodium and chloride, and the formation of bicarbonate into the posterior chamber have been studied in normal dogs, and following complete inhibition of carbonic anhydrase by acetazolamide, 50 mg. per kilogram. Sodium accession approximated fluid formation rate and was reduced 30 per cent by acetazolamide. Bicarbonate formation was reduced to one-third the control value by the inhibitor; chloride was unaffected. Reduction of accession was 1.9 mM per minute for sodium and 1.6 mM per minute for bicarbonate, showing that these are stoichiometrically linked. These results, together with other data in fish and rabbit, support the idea that bicarbonate formation is a general function of ciliary epithelia and, through its effect on sodium, is the basis for a considerable component of fluid movement into the eye. Inhibition of bicarbonate formation appears to be the pharmacological basis for the treatment of glaucoma by carbonic anhydrase inhibitors.