OBJECTIVE： To study the ADR mechanism of conjunctival hyperemia in model rats with prostacyclin-induced high intraocular pressure. METHODS： 50 rats were randomly divided into normal control group， model group， prostacyclin low-dose， medium-dose， high-dose groups （100， 200， 400 mg/kg）， 10 in each group. Except for normal control group， right eyes of rats in other groups were established high intraocular pressure model， dropping corresponding medicine once a day， for 1 week. After last administration， the right eyes cornel peripheral corneal endothelial cells of rats in each group were isolated in vitro and cultured. Vascular endothelial cell viability， cell apoptosis and proliferation-related factor （Ki-76）， apoptosis-related factors （Bad， Bax）， inhibito of apoptosis-related factors （Bcl-2， Bcl-xl） protein expressions were detected. RESULTS： Compared with normal control group， vascular endothelial cell viability in model group were obviously decreased； apoptosis rate was obviously increased； Bad， Bax protein expressions were obviously enhanced； Bcl-2， Bcl-xl， Ki-76 protein expressions were obviously weakened， with statistical significances （P＜0.05 or P＜0.01）. Compared with model group， vascular endothelial cell viability in prostacyclin low-dose， medium-dose， high-dose groups were obviously decreased； apoptosis rate was obviously increased； Bcl-2， Bcl-xl protein expressions were obviously weakened， with statistical significances （P＜0.05 or P＜0.01）； the Bad， Bax protein expressions in prostacyclin medium-dose， high-dose groups were obviously enhanced （P＜0.05 or P＜0.01）， the other indexes had no statistical differences （P＞0.05）. CONCLUSIONS： Prostacyclin may cause conjunctival hyperemia through promoting the apoptosis of cornel peripheral corneal endothelial cells of model rats with high intraocular pressure and decreasing the cell viability.