In four series, each containing five pigmented rabbits, the therapeutic effects of different anti-inflammatory agents on the laser-induced disruption of the blood aqueous barrier was investigated. Utilizing an argon laser, the peripheral iris of the left eye of each animal was coagulated with a total energy input of 1,000 mJ. The right eyes served as controls. After the coagulation the intraocular pressure was monitored at intervals of 10 min, and the anterior chamber was tapped for analysis of the aqueous humour 100 min after treatment. In a fifth group of five rabbits, aqueous humour was analysed without laser or drug treatment. The protein concentration and the activity of the lactate dehydrogenase were analysed in all samples of aqueous humour. A significant effect on the protection of the blood aqueous barrier could be identified in the eyes pre-treated with indomethacin (2 mg/kg body weight, injected intramuscularly), and in those pre-treated with dexamethasone (12.8 mg/kg body weight, injected intravenously; P less than 0.025%). Pre-treatment with aspirin (20 mg/kg body weight, injected intravenously) also had a protective response in the eyes treated by laser. The significance of the results of clinical treatment is outlined.
The effect of YAG laser iridotomy on the blood aqueous barrier in the rabbit was investigated in 21 eyes. In seven series, each containing three pigmented rabbits, the right eye received a YAG laser iridotomy in the upper nasal quadrant of the peripheral iris under standardized conditions utilizing the Mikroruptor II (Lasag Company, Thun/Switzerland). One of the parameters describing the blood aqueous barrier effects was the intraocular pressure, which was monitored at 10 min intervals. The iridotomy caused significant pressure increases in the treated eyes which was maintained up to 90 min following the laser procedure. The measurement of the protein concentration and the lactate dehydrogenase activity was done at equal time intervals after the iridotomy, on the basis of anterior chamber tapping of the treated eyes and the untreated control eyes. Over a period of 100 min after laser surgery, a positive correlation between time and protein concentration for the treated eyes (r = + 0.86) could be established. The activity of the enzyme lactate dehydrogenase in the treated eyes was increased within 5 min of the trauma, reaching a maximum 45 min after surgery, and the increase in activity level remained 150 min after surgery. The results indicate that the disturbance of the blood aqueous barrier with the YAG laser is not essentially different from that of the argon laser, although tissue damage may be more pronounced.
The response of the blood aqueous barrier to a defined laser trauma was investigated in a series of seven groups with three pigmented rabbits in each group. The peripheral iris of the left eye was treated with the Argon laser (ten spots of 50-microns size with an energy of 100 mJ). The right eyes served as controls. The anterior chambers of both eyes were tapped at given time intervals after the laser coagulation to enable the analysis of the protein content of the aqueous humour and for the assay of the lactate dehydrogenase activity. Within 100 min after laser treatment a positive correlation between time and protein concentration in the anterior chambers of the treated eyes (r=0.77) and in the untreated eyes (r=0.79) was established. There was a significant response on the blood aqueous barrier in the untreated fellow eyes. The activity of the lactate dehydrogenase showed a significant increase 5, 70 and 100 min after laser trauma in the treated eyes only. The laser trauma induced a significant increase (alpha-0.01) in the intraocular pressures of the treated eyes, which persisted up to 70 min after treatment. The clinical implications of these findings are discussed.
The therapeutic effect of topically applied prostaglandin inhibitors on the laser-induced disruption of the blood-aqueous barrier was investigated in six series of five rabbits each. One series was not coagulated and served as baseline, and in a reference group laser coagulation was performed without pretreatment with a prostaglandin inhibitor. In four series the iris laser coagulation of the left eyes was preceded by topical application of a prostaglandin inhibitor. The right eyes served as controls for the contralateral effect on the blood aqueous barrier. After laser coagulation the intraocular pressure was monitored at 10-min intervals, and the anterior chamber was tapped for analysis of the protein concentration and the lactate dehydrogenase activity. Pretreatment with dexamethasone eyedrops and indomethacin eyedrops markedly blocked the laser-induced disruption of the blood-aqueous barrier. The level of protein concentration in the aqueous humor after laser coagulation was much less after pretreatment with dexamethasone or indomethacin eyedrops. The effect was significant, both for the laser-treated eyes and for the noncoagulated fellow eyes (p less than 0.025). The subconjunctival pretreatment with dexamethasone 1 or 24 h before laser coagulation had no significant effect with respect to the protection of the blood aqueous barrier.
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