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ABSTRACT. Chronic sequelae of neonatal hyperoxia was studied in male rats exposed to 0.96-1.0 Fi02 for the first 8 days of life. At 58 days of age functional and morphologic cardiopulmonary changes were compared with controls. Right ventricular systolic pressure was measured percutaneously under anesthesia and was increased in the O2 group (29.5 mm Hg f 3.1 versus 23.2 mm Hg f 3 . 5 ,~ < 0.001).Lung and heart weights were similar between groups. Right ventricular weights however were increased in the O2 group (0.197 g f 0.023 versus 0.175 g f 0.020, p < 0.001). Air pressure-volume curves were similar but in the O2 rats saline deflation curves were shifted left and maximal fluid lung volumes were greater (14.1 f 1.2 versus 12.0 f 0.7 ml, p < 0.001). Pulmonary arteries were perfused at 100 cm H 2 0 with a barium-gel mixture and lungs were fixed at 25 cm H 2 0 with formalin. Microscopic examination of lungs revealed dysplastic changes of alveolar architecture which included irregularly enlarged alveoli and incomplete alveolar septation. Morphometric studies of the lungs showed that the Oz rats had an increased volume proportion of parenchyma (0. MLV14, maximal saline lung volume at 14 cm H 2 0 transpulmonary pressureExposure of the lung to increased concentrations of inspired oxygen is associated with multiple toxic effects. These include pulmonary endothelial damage, intraalveolar hemorrhage, development of pulmonary edema, and decreased pulmonary compliance (1-5). The neonate tolerates exposure to hyperoxia with less acute injury than does the adult (6-14). To the neonate, however, hyperoxia presents additional risks by threatening normal growth and development of the lung. In tissue culture, hyperoxia inhibits the growth and extension of pulmonary endothelial tissue (15). In vivo, hyperoxia has been associated with decreased DNA synthesis, decreased lung growth, delayed maturation of alveolar structures, and dysplastic pulmonary vascular development (12,13,(16)(17)(18)(19)(20).The dose and timing dependent relationships of oxygen-induced pulmonary injury are not entirely clear. Long-term sequelae of neonatal hyperoxia exposure have only recently been investigated. Roberts el al. (19) exposed newborn rats to hyperoxia for the first 6 days of life and studied pulmonary changes during the following 2 wk. Abnormalities in lung growth and morphology were initially apparent but became attenuated during the observed recovery period. By 2 wk of recovery the lungs were similar to controls in most respects. However, Wilson et al. (20) investigated the long-term sequelae of prolonged hyperoxia exposure in the young rat.Oxygen exposure was begun at 10 days of age and continued for 2-8 wk. Neonatal hyperoxia exposure for as brief a period as 2 wk was found to be associated with impaired alveolar growth and vascular abnormalities in the adult. These investigations suggest therefore that pulmonary growth abnormalities may accompany either acute or prolonged hyperoxia exposure. The results of these studies differ, however, rega...