[Neuroprotection with carotenoids in glaucoma]. / Neuroprotectia prin carotenoizi în glaucom.

PURPOSE: The aim of the paper was to assess the place of the natural carotenoids (lutein, zeaxanthin) in glaucoma optic neuropathy. METHODS: For this purpose, we carried out an experimental and prospective study, during 3 months, on 8 laboratory animals (Guinea pigs), which we increased the IOP, in both eyes, by cautery of two episcleral vessels. The animals were divided into treatment in two groups: the group I (5 Guinea pigs) which we modified their usual diets by adding 2 cps/day of IcapsL (6 mg lutein/zeaxanthin) and the group II (3 Guinea pigs)--control group, without increasing the diet with lutein and zeaxanthin. The statistical analysis was performed by Student's t test. RESULTS: Before the cautery of episcleral vessels, the mean IOP was 16.8 mm Hg in group I and 16.5 mm Hg in the group II; after the cautery of episcleral vessels, the mean IOP was 26.2 mm Hg in group I and 25.9 mm Hg in the group II (p = 0.004). At the end of the study, the levels of serum lutein were 0.64 mumol/L in group I and 0.22 mumol/L in group II. The loss of retinal ganglion cells was 18.9% in group I and 29.7% in martor group, in correlation with the cup/disc ratio: 0.37, respectively 0.51. Also, in the group II, the increase of IOP was associated at the myelin portion of optic nerve head with axonal degeneration in peripheral regions. CONCLUSIONS: Glaucoma optic neuropathy has a multifactorial pathogenesis, including the oxidative stress. Lutein and zeaxanthin, with its strong antioxidative effects, can represent a viable solution in the complex treatment of glaucoma.

[The role of Brinzolamide 1% ophtalmic suspension in corneal edema]. / Utilizarea suspensiei de Brinzolamida 1% în edemul corneean--studiu experimental pe animale de laborator.

PURPOSE: The study is aimed at assessing the efficacy and safety of topical carbonic anhydrase inhibitor (IAC--i.e. ophthalmic suspension of brinzolamide 1%--Azopt) in the treatment of corneal edema. METHOD: For this purpose, we carried out an experimental, epidemiological-operational, randomised, placebo-controlled and double blind study, on three groups of laboratory animals (rabbits): group 1 (5 rabbits) included endothelial corneal injuries inflicted by ultrasound exposure by means of a phacoemulsification sound in both eyes group 2 (5 rabbits) included endothelial corneal injuries inflicted by direct trauma in both eyes group 3 (3 rabbits)--no endothelial corneal lesions (control group) In each group we instilled, all the animals, with ophthalmic suspension of brinzolamide 1% (Azopt), 1 drop t.i.d., in one eye for 14 days (starting the following day after infliction of endothelial injuries, when the corneal edema was evidenced by biomicroscopic examination) and placebo (saline solution 0.9% with the same osmolar and pH values as the Azopt) in the other eye. The assessment was performed throughout the following stages: To: preceding the infliction of corneal endothelial injuries, resorting to: biomicroscopic examination ultrasound pahimetry direct specular microscopy T1: the following day after infliction of corneal endothelial injuries, resorting to: biomicroscopic examination (the assessment of corneal edema) ultrasound pahimetry (measurement of corneal thickness and, hence edema) direct specular microscopy (cell density and endothelial ultrastructure evaluation: cellular polimegetism, pleiomorphism) T2: in the wake of 14 days therapy (after eye removal), adding to the previous examinations: indirect specular microscopy (with the same aim as the direct examination, yet examination carried out from the endothelial side) pathologic examination (using hematoxilin-eosin dye and Van-Gieson dye).