To study the effect and therapeutically role of octreotide on retinal neovascularization. (1) Forty one-week-old mice were randomly divided into five groups, in which four groups were exposed to 75% oxygen to establish a model of retinal neovascularization, the other group were fed in the normal environment. Mice in control group did not receive any treatment. The two experimental groups were given acetate octreotide by subcutaneous injection at the dose of 20 microg.kg(-1) and 50 microg.kg(-1) respectively twice a day for five days while the control group was given sterile PBS subcutaneously. (2) The mice were sacrificed on 17-day, the eyes were enucleated for histological examination using light and electron microscopy. (3) The effect of acetate octreotide on retinal vessels formation was assessed by counting the number of endothelial cells of new vessels extending from retina to vitreous of 4 microm sagittal retinal cross sections under the light microscope. The expression of SSTR2 in the mice retina was determined by situ hybridization. The change of retinal ultrastructure was observed under the electron microscopy. (1) HE staining: The numbers of endothelial cells of new vessels extending form retina to vitreous in the experimental groups were much less than the control and hyperoxia group (P < 0.01). (2) Situ hybridization showed that SSTR2 expressed in the nurtroganglion layer, endothelial cells and inner nuclear layer in the normal, control and hyperoxia group while the octreotide treated retina showed only light positive staining of SSTR2 in the nurtroganglion layer. (3) Electron microscopy showed hypoxia caused the damage of photoreceptor cells but the damage abated considerably after the mice were treated by the octreotide. Subcutaneous injection of octreotide may suppress the retinal neovascularization in the mice oxygen model and provide some of protection from the damage of retinal ultrastructure.