Optic nerve pH and PO2: the effects of carbonic anhydrase inhibition, and metabolic and respiratory acidosis. 
Earlier studies have demonstrated that carbonic anhydrase inhibitors (CAIs) increase optic nerve oxygen tension (ONPO(2)) in pigs.  We hypothesized that the mechanism of this effect was either a CO(2) increase or a pH decrease in tissue and blood.  To test this hypothesis we investigated and compared how optic nerve pH (ONpH) and ONPO(2) are affected by: (1) carbonic anhydrase inhibition; (2) respiratory acidosis, and (3) metabolic acidosis.  We measured ONpH with a glass pH electrode and ONPO(2) with a polarographic oxygen electrode.  One of the electrodes was placed in the vitreous cavity 0.5 mm over the optic nerve in the eyes of domestic pigs.  We measured ONpH during carbonic anhydrase inhibition and ONpH or ONPO(2) during NH(4)Cl-induced metabolic acidosis and during CO(2) breathing (respiratory acidosis).  Baseline ONpH was 0.12 +/- 0.06 lower than arterial pH (mean +/- SD, n = 10, p < 0.001).  Optic nerve pH decreased with arterial pH during carbonic anhydrase inhibition, metabolic and respiratory acidosis.  Optic nerve oxygen tension was not affected by metabolic acidosis but increased during CO(2) breathing, as it has been shown to do during carbonic anhydrase inhibition.  There is a close correlation between arterial blood pH and intraocular pH. Isolated ONpH changes do not affect ONPO(2), thus the ONPO(2) increase seen with carbonic anhydrase inhibition is probably not only due to pH changes in the blood and optic nerve.  Accumulation of CO(2), either alone or in combination with a pH change, is likely to cause the ONPO(2) increase, but a direct vascular effect should also be considered.