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Retinal and optic nerve oxygen tension increased with systemic administration of dorzolamide. The retinal vessels dilated, probably causing increased blood flow inducing the observed increase in RPO2. The increased oxygenation of retina by CAI may offer therapeutic possibilities in ischaemic diseases of the retina and optic nerve.

An impaired CBF autoregulation can be restored by hyperventilation at a PaCO2 level of about 2.9 to 4.1 kPa (22 to 31 mm Hg). However, it is uncertain whether the restoring effect can take place at lesser degrees of hypocapnia. In the current study, CBF autoregulation was studied at four PaCO2 levels: 5.33 kPa (40 mm Hg, normoventilation), 4.67 kPa (35 mm Hg, slight hyperventilation), 4.00 kPa (30 mm Hg, moderate hyperventilation), and 3.33 kPa (25 mm Hg, profound hyperventilation). At each PaCO2 level, eight rats 2 days after experimental subarachnoid hemorrhage (SAH) and eight sham-operated controls were studied. The CBF was measured by the intracarotid 133Xe method. The CBF autoregulation was found to be intact in all controls but completely disturbed in the normoventilated SAH rats. However, by slight hyperventilation, CBF autoregulation was restored in seven of eight SAH rats with a decline in CBF of 10%. The CBF autoregulation was found intact in all of the moderately or profoundly hyperventilated SAH rats, whereas the decline in CBF was 21% and 28%, respectively. In conclusion, hyperventilation to a PaCO2 level between 4.00 and 4.67 kPa (30 to 35 mm Hg) appears to be sufficient for reestablishing an impaired autoregulation after SAH.

ABSTRACT.Purpose: 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. Methods: 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). Results: Baseline ONpH was 0.12 ± 0.06 lower than arterial pH (mean ± SD, n ¼ 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. Conclusions: 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.