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the neonatal fetal lamb pulmonary circulation after chronic exposure to hyperoxia. To assess the hypothesis that the functional
damage to the pulmonary endothelium after exposure to hyperoxia is due to a time-related reduction in the selective retention ofendothelial-derived extracellular matrix proteins, we exposed neonatal lambs (36 to 39 days gestation; n = 8) for 24 hr tohyperoxia (250 kPa) and then measured both the retention of 125I-labeled albumin (A) and the distribution of thesubendothelial reticular lamina (SL) in the pulmonary arterioles. In comparison to A, the radioactivity associated with SL (B)remained unchanged. Measurements of the morphology (microscopic observations) of the pulmonary arterioles indicated thatthe elastic fibers in these vessels were preserved and that the numbers of both open and closed capillaries was unaltered in thelungs after 24 hr exposure to hyperoxia. This study demonstrates that, although exposure to hyperoxia for 24 hr decreased theselective retention of 125I-labeled albumin, the lack of morphological evidence for endothelial damage suggests that the damage
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