Obiectives To provide suitable animal model (hyperoxia-induced premature rat lung damage) for research of bronchopulmonary dysplasia (BPD) and to better understand pathogenesis of BPD and look for effective drugs to prevent and treat BPD.Methods Rat litters delivered prematurely at 21-day gestation by hysterotomy. Vigorous resuscitation at birth resulted in a high survival rate. Surfactant and antioxidant enzyme (AOE) system were measured. The model was tested in an experiment of hyperoxia-induced lung injury. Results Compared to litters delivered spontaneously at term (gestation 22 days), these preterm rats had immature pulmonary surfactant composition with low total phospholipid (□±s: 10.09±1.49 μg/mg wet weight vs 12.04±1.31 μg/mg wet weight; P=0.0367) and phostidylcholine (5.06±1.82 μg/mg wet weight vs 8.28±2.35 μg/mg wet weight; P=0.0238) levels. The concentrations of AOE enzymes, superoxide dismutase (11.40±2.04 μ/mg DNA vs 15.78±1.84 μ/mg DNA; P<0.01) and catalase (92.81±62.25 μ/mg DNA vs 412.24±117.50 μ/mg DNA; P<0.01) were also significantly lower. Animals exposed to hyperoxia had a significantly higher mortality. Pulmonary edema and histological features of lung damage were observed in the pups exposed to hyperoxia. Conclusions The premature rat model is relatively cheap, readily available and has a high survival rate. Pulmonary surfactant and AOE systems are immature. These properties make them a suitable model for the study of acute and chronic lung damage related to prematurity and O2 toxicity.