Restoration of damaged hepatocytes after ischemia was studied functionally and morphometrically in a rat model with partial hepatic vascular occlusion. In 30 min occlusion group (n = 35), ATP (mols/mg of protein) dropped down to nearly zero, but returned to the pre-ischemic level within 6 hours after reperfusion. The number of mitochondria (Mt)/unit area of cytoplasm (N/beta m2) increased to 1.41 times of the pre-ischemic value. Simultaneously, the area of single Mt decreased to 2/3 of the pre-ischemic value. Cellular necrosis and subsequent fibrosis were slight, not different from those of the controls. In 60 min occlusion group (n = 35), it took 14 days for ATP to return to the pre-ischemic level. An increase in the number of Mt and reduction in the Mt area, were slight compared with 30 min occlusion group. In contrast, necrosis and subsequent fibrosis markedly developed with a concomitant increase in lysosomes. In conclusion, it was suggested that, in 30 min of ischemia, active division of Mt, which is a compensatory mechanism of Mt reduced the degree in ischemic damage of hepatocytes, in contrast, in 60 min ischemia, division of mitochondria was limited, causing delayed recovery of ATP and severe necrotic change of hepatocytes.