dinoprost and Endophthalmitis

Lens protein-induced ocular inflammation in rabbits was used to study the action mechanism of some anti-inflammatory agents. Indomethacin, a cyclooxygenase inhibitor, markedly reduced PGE2 and PGF2 alpha in the iris and ciliary body at 2 h but PGE2 only at 4 h. REV 5901, a lipoxygenase inhibitor, only significantly reduced PGE2 levels in the ciliary body at 4 h. PGF2 alpha levels were not affected by REV 5901. When indomethacin and REV 5901 were combined, both PGE2 and PGF2 alpha were suppressed at 2 and 4 h in both iris and ciliary body. Neither matrine nor prednisolone produced significant effects on the levels of PGE2 and PGF2 alpha. However, prednisolone exhibited the greatest reduction in chemotaxis of leukocytes followed by REV 5901. Indomethacin, on the contrary, produced a significant increase in chemotaxis of leukocytes. Matrine produced a decrease in leukocyte counts but was not statistically significant. These results indicate that indomethacin is effective in the early phase of inflammation to reduce PG's production whereas prednisolone and REV 5901 were more effective in the late phase of inflammation. Combined use of REV 5901 and indomethacin could become a drug of choice for the treatment of ocular inflammation without inducing corticosteroidal side effects.

Topics: Alkaloids; Animals; Anti-Inflammatory Agents, Non-Steroidal; Chemotaxis, Leukocyte; Dinoprost; Dinoprostone; Endophthalmitis; Female; Indomethacin; Lipoxygenase; Lipoxygenase Inhibitors; Male; Matrines; Prednisolone; Quinolines; Quinolizines; Rabbits

Three hours to 14 days following the intravitreal injection of 10 ng of E. coli endotoxin into the vitreal chamber of one eye of the New Zealand white rabbit, ocular inflammation was evaluated by clinical and biochemical criteria and prostaglandins were measured in the intraocular fluids and in the incubation medium of the intact lens. Increased synthesis of PGE2 was detected for lenses from inflamed eyes beginning at 18 h post-endotoxin injection. Lenticular PGE2 synthesis remained above control levels for the duration of the time course. Lenses also exhibited increased PGF2 alpha synthesis, which began at 18 h and returned to control levels by day 7. At the times of peak production, aqueous humor PGE2 concentration correlated with lenticular PGE2 synthesis and with aqueous humor leukocyte number. No correlations were found for lenticular PGE2 vs. cell number, or vitreous humor PGE2 vs. aqueous humor PGE2. These results suggest that during ocular inflammation, aqueous humor PGE2 may be derived, at least in part, from the lens and leukocytes.

Topics: Animals; Body Fluids; Dinoprost; Dinoprostone; Endophthalmitis; Endotoxins; Escherichia coli; Lens, Crystalline; Male; Prostaglandins E; Prostaglandins F; Rabbits