Elevated vitreous nitric oxide levels in patients with proliferative diabetic retinopathy.

PURPOSE: The aim of this study was to determine nitric oxide levels in the vitreous of patients with proliferative diabetic retinopathy. METHODS: Using the spectrophotometric method based on Griess reaction, we measured levels of nitrite, the stable product of nitric oxide, in the vitreous of 21 eyes of 21 patients who underwent vitrectomy for the treatment of proliferative diabetic retinopathy with tractional retinal detachment, prospectively. Three samples were excluded from the study because of blood contamination. The control group was made up of vitreous samples from 15 eyes of 15 normal cadavers and five eyes of five patients who were undergoing vitrectomy for macular hole surgery. RESULTS: Nitrite levels were 0. 524 +/- 0.27 microM and 0.383 +/- 0.17 microM in the vitreous of patients with proliferative diabetic retinopathy of diabetes type I and type II, respectively. In 15 cadaver eyes and five vitreous samples from patients who underwent macular hole surgery, nitrite levels were below the detection limit (less than 0.08 microM). There was no significant difference between nitrite levels in patients with type I and type II diabetes (P =.56), whereas there was a significant difference between diabetes groups and controls (P <. 00001). CONCLUSION: Vitreous nitric oxide levels are elevated in patients with proliferative diabetic retinopathy with tractional retinal detachment. Nitric oxide may play a role in the pathogenesis of proliferative diabetic retinopathy.

Effect of nitric oxide on proliferation of human retina pigment epithelial cells.

PURPOSE: To investigate the effects of exogenous and endogenous nitric oxide (NO) on the proliferation of human retina pigment epithelial (RPE) cells. METHODS: We stimulated cultured human RPE cells with 3-morphosydnonimine (SIN-1) to analyse the effect of exogenous NO. Incubation with a cytokine cocktail (interleukin 1-beta + interferon gamma + tumour necrosis factor alpha) plus lipopolysaccharide (LPS) induced cells to synthesise NO endogenously. The cultures were then incubated for 48 h, after which the cells were stained with crystal violet and absorbance at 550 nm was measured spectrophotometrically. RESULTS: SIN-1 inhibited human RPE cell proliferation, while haemoglobin, an NO inhibitor, almost completely blocked the inhibitory effect. On the other hand, treatment with the cytokine cocktail plus LPS did not inhibit RPE cell proliferation. CONCLUSION: These findings confirm that exogenous NO inhibits human RPE cell proliferation, while endogenous NO has no such blocking effect.