OPTIC NERVE OXYGEN TENSION – EFFECT OF INTRAOCULAR PRESSURE AND GLAUCOMA MEDICATION

E. Stefánsson, P. Koch-Jensen. T. Eysteinsson, K. Bang, Jens F. Kiilgaard, A. Wiencke, J. Dollerup, D. Bach Pedersen and M. laCour

University of Iceland, Iceland and University of Copenhagen, Denmark

Purpose:

To evaluate the effect carbonic anhydrase inhibitors have on the optic nerve oxygen tension (ONPO₂) and to study the relationship between intraocular pressure (IOP) and ONPO₂.

Methods:

Polarographic oxygen electrodes were placed in the vitreous cavity over the optic nerve head in anaesthetised pigs. Acetazolamide and dorzolamide were administered intravenously or topically. IOP was controlled with a cannula in the anterior chamber connected to a saline reservoir.

Results:

Intravenous dorzolamide and acetazolamide raised the ONPO₂ in a dose dependent fashion. This was seen with intravenous doses between 6 and 500 mg as well as with topical application of dorzolamide eye drops.

Intravenous injections of 500 mg of dorzolamide raise the ONPO₂ from 16+/-6 mmHg to 27+/-12 mmHg (n=5, mean+/-SD, p= 0.017), and 500 mg of acetazolamide raised ONPO₂ from 24+/-10 to 31+/-10 mmHg (n=6, p=0.001). Optic nerve blood flow increased simultaneously with the increasing ONPO₂. Topically applied Trusopt ® eye drops raise the ONPO2 by 11%. IOP affects ONPO₂. When IOP is normal or moderately elevated the ONPO₂ is autoregulated and unchanged and falls linearly when IOP goes above 30-40 mmHg. Dorzolamide affects ONPO₂ at normal and elevated levels of IOP.

Conclusion:

In animal models, carbonic anhydrase inhibitors affected optic nerve oxygen tension through a dual mechanism. Acetazolamide and dorzolamide elevate the optic nerve oxygen tension directly, presumably through a vasodilatory effect, and indirectly through lowering the intraocular pressure. This effect was seen with topically and intravenously applied dorzolamide.