Immaturity and oxygen toxicity have been implicated in the pathogenesis of the neonatal disease bronchopulmonary dysplasia. The present study aimed to investigate the use of magnetic resonance imaging (MRI) to assess hyperoxia-mediated lung injury in the term and premature neonate. Term (gestation, 22 d) and premature (21 d) rat pups were exposed to hyperoxia (Ͼ95%) or air for a 6-d period (n ϭ 7) and assessed for lung damage by MRI. Pulmonary signal intensities of T 1 -weighted images were significantly increased in both hyperoxia-exposed term and premature neonates, relative to air-breathing controls (p Ͻ 0.01). T 2 -weighted MRI signal intensities were also greater in premature and term rat pups exposed to hyperoxia, but failed to reach significance (p Ͼ 0.05). Elevated MRI pulmonary signal intensities may have represented an increase in magnetic resonance-detectable free water, possibly indicating an increase in edema. Corresponding histologic evidence of lung injury was detected in both term and premature rat pups exposed to hyperoxia. Histologic samples indicated focal regions of alveolar hemorrhage, immune cell infiltration, edema, and collapse in both term and premature rat neonates exposed to hyperoxia. Alveolar air space was assessed (n ϭ 5) by light microscopy within a 0.5 mm 2 region of the superior left and inferior right pulmonary lobes of each treatment group. Alveolar area of the superior left lung lobe of the premature hyperoxia treatment group was significantly smaller than other treatment groups (p Ͻ 0.05). Reduced area for respiratory exchange was probably a result of observed focal areas of edema and collapse. MRIdetectable increases in lung signal intensity may have represented an increase in hyperoxia-induced pulmonary edema in the 6-d-old rat neonate. Increases in signal intensity correlated with the appearance of edema in pulmonary histologic samples. Premature delivery had a less defined effect on lung injury but possibly exacerbated hyperoxia-mediated pulmonary damage. Normal pulmonary growth and development are disrupted at premature birth. In the premature human neonate, ventilation with elevated oxygen concentrations is often required to correct hypoxemia at room air. Hyperoxia has been implicated in the development of both RDS and BPD (1). Pulmonary oxygen toxicity has been studied in a number of species (2-4) and tends to develop into two well-described stages, representing a transition from acute to chronic lung injury. The initial acute phase involves the accumulation of proteinaceous edema and the development of fibrin-rich membranes, whereas chronic injury is characterized by metaplasia, immune cell infiltration, and fibrosis (5). Examples of hyperoxia-induced changes in pulmonary architecture have been documented in the adult (6), immature rat (7,8), and the neonatal rat pup (9).MRI is primarily based on the detection of a signal from the hydrogen nuclei of water owing to the magnetic properties of water molecules when exposed to a magnetic field. Therefore, an increase in ...