Nicardipine Inhibits Acute Rise of Aqueous Flare and Intraocular Pressure Induced by Argon Laser Photocoagulation

Abstract

The purpose of this study was to examine the anti-inflammatory effect of the calcium channel blocker nicardipine. Intraocular inflammation was induced by argon laser photocoagulation of the iris of pigmented rabbits and was assessed by measuring aqueous flare and intraocular pressure. This resulted in a marked increase in the aqueous flare that peaked at approximately one hour following coagulation and returning to the original values after six hours. Intraocular pressure increased within 15 minutes following laser treatment and returned to baseline levels at 60 minutes. Pre-treatment of the rabbits with an intravenous injection of 2 mg/kg of nicardipine completely abolished both the increase in aqueous flare and intraocular pressure induced by laser photocoagulation as compared to the control experiment. Earlier work from the author's group has shown that nicardipine can also block aqueous flare and intraocular pressure increases induced by topical administration of prostaglandin E2. From these combined experiments they would like to draw the conclusion that the inflammatory reaction induced by photocoagulation of the iris is partly mediated by prostaglandins and that blockade of calcium channels by nicardipine can inhibit the effects induced by prostaglandin E2.

Nilvadipine Inhibits Acute Rise of Aqueous Flare and Intraocular Pressure Induced by Prostaglandin E₂ in Pigmented Rabbits

“…We also reported that intravenous nicardipine, 2 mg/kg body weight, inhibited the acute rise of aqueous flare and intraocular pressure induced by argon laser photocoagulation in pigmented rabbits [3]. We further showed that when 50 Ìg/ml of PGE 2 was applied every day for 6 days, the flare intensity decreased significantly day by day [4].…”

“…The measurement was taken in the midportion of the anterior chamber. The sampling area was 0.075 mm 3 . Aqueous flare elevation is expressed as the area under the curve (AUC) and inhibition is estimated by the following equation: Those who carried out the measurements were not informed about the treatment.…”

Inhibitory Effect of Nilvadipine on Disruption of Blood-Aqueous Barrier Induced by Prostaglandin E₂ Application in Pigmented Rabbits: A Morphologic Study

“…Not all calcium channel blockers inhibit the acute rise of aqueous flare induced by PGE 2 in rabbits [3][4][5]. Chang et al [8] reported that nifedipine and nisoldipine (calcium channel blockers) inhibited the activity of phospholipase A 2 in a cell-free preparation of human platelets that acts on the release of arachidonic acid.…”

“…Several investigators demonstrated that some kinds of calcium channel blockers inhibit the experimental inflammation: Kaji et al [3,4] showed that intravenously administered nicardipine (a calcium channel blocker), 2 mg/kg body weight, inhibited the acute rise of aqueous flare induced by PGE 2 and laser irradiation to the iris. Nilvadipine, 5-isopropyl-3-methyl-2-cyano-1,4-dihydro-6-methyl-4-(m-nitrophenyl)-3,5-pyridinedicarboxylate, is another calcium channel blocker and is clinically used for the treatment of systemic hypertension.…”

Effects of Nilvadipine, Nicardipine and Verapamil on Acute Rise of Aqueous Flare Induced by Iris Photocoagulation or Intravenous Lipopolysaccharides in Pigmented Rabbits

“…In 1994, Kaji et al [1] showed that nicardipine, 1,000 Ìg/kg, suppressed the prostaglandin-E 2 -induced flare elevation. In 1996, Kaji et al [2] demonstrated that nicardipine, 2,000 Ìg/kg, inhibited the photocoagulation-induced flare rise. In 1998, Zhang et al [3] reported that nilvadipine, 5-500 Ìg/kg, inhibited the PGE 2 -induced flare elevation.…”