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E.C. LaHey, R.M. H. Diederen, N. Deutz, S.C. Dieudonne, A.T. A. Liem, A. Kijlstra, F. Hendrikse; Increased Nitric Oxide Pathway Metabolites During Retinal Detachment . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5585.
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Purpose: The aim of our study was to examine whether rhegmatogenous retinal detachment (RRD) is associated with increased levels of nitric oxide (NO), citrulline and arginine. Methods: Undiluted vitreous samples were obtained from 151 patients undergoing pars plana vitrectomy. Vitreous concentrations of 2 amino acids, citrulline and arginine were determined by high–pressure liquid chromatography (HPLC). Using the HPLC method we also measured levels of nitrite, the stable product of NO. The study group consisted of 93 patients (93 eyes) with a rhegmatogenous retinal detachment (RRD). The control group consisted of vitreous samples from 25 eyes with an idiopathic macular hole and 24 eyes with an idiopathic epiretinal membrane. Vitreous from eyes with a traction retinal detachment (n=9) due to proliferative diabetic retinopathy (PDR) was also investigated. Results: The mean vitreous concentration of citrulline and arginine was significantly increased in eyes with RRD (9.6±4.3 and 97.2±29.2; respectively) compared to control eyes (7.1±3.2 and 75.9±18.1; respectively) (P= 0.034 and P= 0.002; respectively). Also the mean concentration of nitrite was higher in vitreous of patients (2.24±1.4) compared to controls (2.01±0.72; P=0.058). In addition, a positive correlation was found between vitreous concentration of citrulline and arginine and pre–operative visual acuity (P=0.001 for both amino acids). The mean vitreous concentration of citrulline, arginine and nitrite was significantly elevated in eyes with PDR (25.8±10.3; 130.7±23.7; 2.21±1.53; respectively) compared to control eyes (P=<0.001; P= 0<001; P=0.004, respectively). Conclusions: Increased nitric oxide pathway metabolites were found in eyes with rhegmatogenous retinal detachment. This increase may be related to the retinal hypoxia and NO may play a role in the pathogenesis of photoreceptor damage after retinal detachment.
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