Affiliations: CEMOT, University of Bari, Italy | Department of Ophthalmology University of Bari, Italy | DETO, University of Bari, Italy
Note: [] Corresponding author: Giuseppe Cicco, MD, CEMOT, Università degli Studi di Bari, piazza G. Cesare, 11 70124 Bari, Italy. Tel./Fax: +39 080 5478156; E-mail [email protected].
Abstract: Background: Glaucoma is currently attributed to two different possible pathogenetic mechanisms: mechanical (the ocular damage is induced by physical injury), and vascular (the ocular damage is sustained by ischemia of the optic nerve head). Aim: We considered the possibility that several anti-glaucoma drugs (β-blockers, carbonic anhydrase inhibitors and prostaglandins) could have an influence on optic nerve head hemorheology and oxygen supply. Materials and method: We studied 4 groups of 10 subjects each: a control group, and 3 primary open angle glaucoma (POAG) groups, treated with topical β-blockers, (10 patients), carbonic anhydrase inhibitors (CAI), and prostaglandin analogs (PG), respectively. In these 4 groups we investigated the RBC surface AchE and cytosolic calcium levels in order to assess their possible influence on the hemorheology and microcirculation in optic nerve head blood perfusion. Results: A significant correlation (p<0.048) was found between the RBC surface acetylcholinesterase and RBC intracytosolic calcium values in patients with POAG treated with β-blockers. We found no significant correlation (p=n.s.) between the same patterns in the other Groups or in Controls. Conclusion: These data indicate that CAI and PG drugs do not interfere with AchE in POAG patients, whereas β-blockers negatively affect the RBC deformability.
