Corticosteroid treatment of laser retinal damage affects prostaglandin E₂ response

The current study investigated the effect of steroid treatment of eyes subjected to a single retinal argon laser lesion on vitreal accumulation of both prostaglandin E₂ (PGE₂) and protein and their relationship with the amounts of PGE₂ released from the retina-choroid. Laser exposure resulted in an elevation in the amounts of PGE₂ released by the retina-choroid of laser-treated eyes: there was an initial peak on day 1, followed by a higher peak on day 7 (13.0 ± 3.9 ng/mg protein and 32.9 ± 4.9 ng/mg protein, respectively) after which levels progressively declined. Steroid treatment prevented the initial peak, but did not prevent the enhanced PGE₂ amounts released during the second week. Thus, on day 7 the amounts released were lower by 32% than in the untreated group (21.0 ± 8.6 ng/mg protein vs 32.9 ± 4.9 ng/mg protein, P = 0.000); by day 14, however, peak values in the treated group were higher than in the untreated group (32.2 ± 12.4 ng/mg protein and 10.6 ± 4.5 ng/mg protein, respectively). In steroid-treated eyes, vitreal PGE₂ concentration remained unchanged from baseline over a 2-week follow-up, whereas in the untreated laser group, levels peaked on day 7 to 10.7 ± 3.6 ng/ml, exceeding baseline levels of 5.8 ± 1.7 ng/ml (P = 0.0002). Laser exposure was also associated with a biphasic elevation in vitreal protein concentrations on days 3 and 14 (0.68 ± 0.16 mg/ml and 0.79 ± 0.13 mg/ml, respectively); these were significantly higher than the baseline value of 0.43 ± 0.12 mg/ml (P = 0.03 and P = 0.004, respectively). Steroid treatment resulted in a single elevation of vitreal protein concentration, occurring on day 7, when values reached 1.00 ± 0.31 mg/ml. Our study demonstrated that steroid treatment of laser-induced retinal damage transiently reduced the amounts of PGE₂ released from the laser exposed retina-choroid. This inhibition occurred during the initial phase after exposure; at the later phase, augmented release was resumed. In addition, this treatment affected vitreal PGE₂ and protein concentrations selectively; the accumulation of PGE₂ above baseline was completely prevented while that of protein was lowered only partially.