Exposure to cyclic oxygen sufficient for development of oxygen-induced retinopathy does not induce bronchopulmonary dysplasia in rats.

Bronchopulmonary dysplasia and retinopathy of prematurity affect premature infants exposed to supplemental oxygen. Susceptibility to oxygen-induced retinopathy in the rat is heritable, with inbred Dark Agouti (DA) rats being more susceptible than Fischer 344 (F344) rats. To establish if hyperoxic exposure sufficient to induce florid retinopathy would induce strain-specific lung changes, newborn DA and F344 rats were exposed to cyclic hyperoxia or room air for up to 18 days. Lung function was assessed at 18 days, and standardized morphometry and immunohistochemistry were performed at intervals. No differences in arterial blood gases or protein concentration of bronchoalveolar lavage fluid were observed amongst groups at 18 days, although lung wet-to-dry weights were significantly lower for F344 than for DA rats. Pulmonary vascularity increased in all oxygen-exposed animals compared with room air-exposed controls, but there was no significant difference between strains. The lung surface area of oxygen-exposed F344 rats was significantly increased at day 10 compared with F344 controls and oxygen-treated DA rats, but at 14 and 17 days the oxygen-exposed DA rats showed increased lung surface area compared with oxygen-exposed F344 rats. The minor morphological differences found in the lung did not affect pulmonary function, suggesting that mechanisms inducing oxygen-induced retinopathy and bronchopulmonary dysplasia are fundamentally different, and that susceptibility to bronchopulmonary dysplasia is not heritable in the rat.