The hemodynamic changes during postischemic reperfusion were investigated in the eyes of young (4 months) and aged (more than 18 months) rats using laser Doppler flowmetry, and histological changes in the retina were examined 6 h after the cessation of ischemia. During exposure to 80 mmHg of intraocular pressure, choroidal blood flow (ChBF) decreased to 40–50% of the baseline value. Marked hyperperfusion (186 ± 9%) was observed 1 min after cessation of 30-min ischemia in young rats. The hyperperfusion was less (111 ± 3%) after 120-min ischemia. Delayed hypoperfusion was not observed during 6 h of reperfusion after 120-min ischemia. In aged rats, the hyperperfusion after 30-min ischemia was less (130 ± 17%) than that in young rats, and the ChBF decreased to 80% of the baseline value during 6 h of reperfusion after 120-min ischemia. Histological examination of the retina showed that exposure to 120-min ischemia caused microvacuolation in the inner and outer plexiform layers and vacuolar changes in the cytoplasms in the inner nuclear layer of both young and aged rats, suggesting edema formation in the retina. The thickness of the outer layers of the retina tended to increase after 120-min ischemia in young rats, whereas it decreased significantly in aged rats. These results suggest that 120-min ischemia with 40–50% of normal choroidal blood flow causes more severe damage than 30-min ischemia, and that the hemodynamic changes during reperfusion in aged rats are different from those in young rats.