Exprimental Study Of The Effect Of Octreotide On Retinal Neovascularization

Objective To study the effect of octreotide on retinal neovascularization and investigate the mechanism. Method Fourty one-week-old Kunming mice were randomly divided into normal group, 75% oxygen treated group, 50ug.kg-l octreotide injected group, 20 g. kg-1 octrotide injected group and 0. 9%NaCl injected group. The normal group were fed in the normal environment. The other four groups were exposed to 75% oxygen to establish a model of retinal neovascularization .Mice in normal group received no treatment. The two octreotide treated groups were given acetate octreotide by intraperitoneal injection at the dose of 20 g. kg-1 and 50 g. kg-1 respectively twice a day for five days while the 0. 9%NaCl injected group was given steriled 0.9% NaCL. The mice were sacrificed on 17-day-old, the eyes were enucleated and processed for histological examination and transmission electron microscopy. The effect of acetate octreotide was assessed by counting the number of endothelial cells of new vessels extending from retina to vitreous of 4 m sagittal retinal cross sections under the light microscope. The expression of SSTR2 in the mice retina was determined by situ hybridization. Result The average number of endothelial cells of new vessels extending from retina to vitreous per eye of every group were 4 in the normal group, 260 in the 75% oxygen treated, 80 in the 50 g.kg-1 octreotide injected group, 139 in the 20 g. kg-1 octrotide injected group and 257 in the 0. 9%NaCl injected group. The number of endothelial cells of new vessels in the octreotide treated group were much less than the 75% oxygen treated group(p<0. 05). SSTR2 expressed in the neutroganglion layer and inner nuclear layer of all the groups. The difference among the five groups was meaningless statistically. By electronic microscopy examination the rod outer segment layer appeared thinner , the rod outer segment was shorter, the discs is partly unclear and vacuolar in the 75% oxygen treated group compared with the normal group .However in the octreotide treated groups the retinal ultrastructurewas intact without overt toxic reaction and the leision in the rod outer segment layer was unobvious . Conclusion Intraperitoneal injection of octreotide had effective inhibition of the retinal neovascularization in the murine model of ischemia-induced retinopathy but little toxicity perhaps through connecting to SSTR2 in the retina. Futhermore, Intraperitoneal injection of octreotide may protect the lesion of retinal ultrastructure caused by hypoxia.