An experimental model of retinal acute photic injury was developed in Wister rats. Aninmls were exposed to white light in intensity of 20 000 lux under general anesthesia for 1 hr. Two rats were sacrificed at 24, 48hr, day 7, 14,21,28,35 after liht exposure respectively. The histopathologic study showed that the retinal acute photic injury initiated in the outer seSment characterized by disorganization and loss of the outer segment at the early stage, and then the inner segment and RPE were involved. The decrease of the thickness of the outer nuclear layer was seen in a few of our cases. Some of our samples showed recovery of the outer and inner segment from the light damage of certian degrees 2 or 3 weeks after light exposure, but others did not. One sample from 5 weeks after light exposure demonstrated that the outer nuclear layer, the outer and inner segment completely lost. Thc inflammatory responses were not observed in all of our samples inplicating that the retinal acute photic damage is a degeneration process. （Chin J Ocul Fundus Dis,1994,10:84-85）