HYPEROXIA-INDUCED LUNG INJURY IN PREMATURE RAT - DESCRIPTION OF A SUITABLE MODEL FOR THE STUDY OF LUNG-DISEASES IN NEWBORNS

Objective To provide suitable animal model (hyperoxia-induced prematur e rat lung damage) for research of bronchopulmonary dysplasia (BPD) an d to better understand pathogenesis of BPD and look for effective drug s to prevent and treat BPD. Methods Rat litters delivered prematurely at 21-day gestation by hysterotomy. Vigorous resuscitation at birth re sulted in a high survival rate. Surfactant and antioxidant enzyme (AOE ) system were measured. The model was tested in an experiment of hyper oxia-induced lung injury. Results Compared to litters delivered sponta neously at tem (gestation 22 days), these preterm rats had immature pu lmonary surfactant composition with low total phospholipid ((x) over b ar s: 10.09 +/- 1.49 mu g/ mg wet weight vs 12.04 +/- 1.31 mu g/mg wet weight; P =0.0367) and phostidylcholine (5.06 +/- 1.82 mu g/mg wet we ight vs 8.28 +/- 2.35 mu g/mg wet weight; P = 0.0238) levels. The conc entrations of AOE enzymes, superoxide dismutase (11.40 +/- 2.04 mu/mg DNA vs 15.78 +/- 1.84 mu/mg DNA; P < 0.01) and catalase (92.81 +/- 62. 25 mu/mg DNA vs 412.24 +/- 117.50 mu/mg DNA; P<0.01) were also signifi cantly lower. Animals exposed to hyperoxia had a significantly higher mortality. Pulmonary edema and histological features of lung damage we re observed in the pups exposed to hyperoxia. Conclusions The prematur e rat model is relatively cheap, readily available and has a high surv ival rate. Pulmonary surfactant and AOE systems are immature. These pr operties make them a suitable model for the study of acute and chronic lung damage related to prematurity and O-2 toxicity.