Effect of vasopressin V1 receptor antagonist on optic nerve blood flow autoregulation in experimental ischemic optic neuropathy

ABSTRACTEffect of Vasopressin V1 Receptor Antagonist on Optic Nerve Blood FlowAutoregulation in Experimental Ischemic Optic NeuropathyAutoregulation of optic nerve head blood flow plays an important role in theetiopathogenesis of ischemic optic neuropathy. In our study, we evaluated the effect ofvasopressin V1 receptor antagonist on biochemical and ultrastructural changes caused byexperimental ischemic optic neuropathy.The study group consisted of 13 rabbits. The subjects were divided into three groups.Group I consisted of 3 rabbits wheras group II and III consisted of 5 rabbits. Group I was thecontrol group. All of the rabbits underwent fundus examination and intraocular pressuremeasurement prior to the experiment, following the formation of retrobulbar haematoma andbefore enucleation. The subjects in group II underwent bilateral enucleation 7 hoursfollowing the formation of retrobulbar haematoma. Group III underwent peribulbar 100 ng/2µl [deamino-Pen1, O-Me-Tyr2, Arg8]-Vasopressin (vasopressin V1 receptor antagonist)injection six hours following the formation of retrobulbar haematoma. We enucleated both ofthe globes one hour after the injection. All of the optic nerves underwent biochemical andhistopathological examination.Intraocular pressure values measured before enucleation were found to be lower ingroup III in comparison to group II, and this was statistically significant (p<0.05). Superoxidedismutase levels were higher in group I than the other two groups (p=0.02). Group II had thelowest superoxide dismutase level. Super oxide dismutase levels in group III were not as highas the levels in group I, but were not as low as the levels in group II. Histopathologicalischemic changes were found to be more prominent in group II, wheras ischemic changeswere found to be regressed in group III.We suggest that vasopressin V1 receptor antagonist can be effective in reducing thebiochemical and ultrastructural changes caused by ischemia.Key Words: Experimental ischemic optic neuropathy, superoxide dismutase,ultrastructural changes, vasopressin V1 receptor antagonist.