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K.R. Russell, J. Carnes; Morphine–Stimulated Nitric Oxide Production in Rabbit Aqueous Humor . Invest. Ophthalmol. Vis. Sci. 2006;47(13):221.
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Recent studies in our laboratory have demonstrated that nitric oxide plays a role in morphine–induced reduction of intraocular pressure and pupil diameter in New Zealand white (NZW) rabbits. The goal of the present study was to determine the effect of morphine on nitric oxide levels in the aqueous humor of NZW rabbits.
Normal, dark–adapted (reverse light cycle, 12/12 hr dark/light) NZW rabbit eyes were treated topically and bilaterally as follows: 1) morphine (100 µg) for 5 or 30 minutes; 2) 30 minute pretreatment with naloxone (100 µg; a nonselective opioid receptor antagonist) or L–NAME (0.5 %; a nitric oxide synthase inhibitor), followed by treatment with morphine for 5 or 30 minutes. Aqueous humor samples were obtained by paracenthesis and immediately assayed for nitric oxide (nitrites + nitrates) using a nitric oxide quantitation kit.
The levels of NO in aqueous humor of rabbits treated with morphine for 5 minutes, increased from 34.22 ± 2.22 µM (control) to 105.19 ± 15.55 µM (treated). Rabbits that were treated with morphine for 30 minutes had no significant changes in aqueous NO levels when compared to control animals. The increase in NO levels by morphine (5 min) was inhibited in the presence of naloxone (100 µg) or L–NAME (0.5%).
Morphine–induced increase in NO levels in aqueous humor is a time–dependent response that is linked to activation of mu–opioid receptors. Data obtained suggest that morphine–stimulated changes in ocular hydrodynamics and iris function are due, in part, to increased release of NO in aqueous humor.
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