Nitric oxide synthase (NOS) expression is increased in the retina of rats subjected to perinatal asphyxia.

REY FUNES, M. E. ; CAPANI, F. ; LOPEZ-COSTA, J. J. ; LOPEZ, E. M. ; BAYONA, J. C. ; HUARTE, M. ; LOIDL, F. C. ; RODRIGO GARCIA, J ; COIRINI, H

New York

Congreso; Meeting of the American Society for Neuroscience; 2004

Retinopathy of prematurity (ROP) is a major cause of blindness in children worldwide. Nitric oxide (NO) has been considered one of the possible factors involved in this pathology. Using a model of perinatal asphyxia (PA) in rat, we have described neovascularization in the internal limitant layer and hypertrophy of Müller cell's processes. These changes resembled those observed in ROP. We have evaluated the NOS in the retina after PA. Retinal sections from 60 days old male rats subjected to 20 min of PA in normothermic condition (PA/37), 20 min of PA in hypothermic (15°C) condition and controls were stained using the histochemical technique to nicotinamide adenine dinucleotide diaphorase (NADPH-d) and a specific neuronal NOS antibody. Using the NADPH-d technique, PA/37 animals showed a hyperplasia of amacrine neurons, augmented cell area and optic density, and retinal neovascularization compared to control. In contrast tissue from hypothermic condition showed a hypoplasy of amacrine neurons with increased reactive area, without changes in optic density. Immunocytochemistry for NOS confirmed this data. This results support the participation of NO in the physiopathology of hypoxia-ischemia of ROP. Since hypothermia revert some of these changes could be an efficient therapeutic agent to avoid the development of ophthalmologic diseases.