Increased nitric oxide synthase activity is essential for electromagnetic-pulse-induced blood-retinal barrier breakdown in vivo.

PURPOSE: To examine whether electromagnetic pulses (EMPs) affected the permeability of the blood-retinal barrier (BRB), gene expression of occludin and activity of nitric oxide synthase (NOS).
METHODS: Sprague-Dawley (SD) rats were used and randomized into EMP and control groups. Retinas were removed immediately, and 2 h or 24 h after EMP radiation. BRB permeability was analyzed by transmission electron microscopy and Evans Blue staining. Retinal NOS activity and concentrations of nitrite and nitrate were measured. Occludin mRNA and protein levels were detected by RT-PCR and Western blotting.
RESULTS: Exposure of SD rats to EMP resulted in increased BRB permeability, with the greatest decrease in occludin at 24 h. Moreover, this permeability defect was also correlated with significant increases in the formation of NO and induction of NOS activity in SD rats. Furthermore, we found that treatment with NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME) blocked BRB breakdown and prevented the increase in NO formation and induction of NOS activity, as well as the decrease in occluding expression.
CONCLUSION: Taken together, these results support the view that NOS-dependent NO production is an important factor that contributes to EMP-induced BRB dysfunction, and suggests that NOS induction may play an important role in BRB breakdown.