Hyperoxic lung injury is a frequent and unfortunate consequence of supraphysiologic oxygen therapy. Relative to adults, newborns of most species are resistant to lung O2 toxicity. However, the development of newborn lung exposed to hyperoxia is profoundly affected with a marked inhibition of normal alveolization. We have previously shown increases in intercellular adhesion molecule-1 (ICAM-1), platelet endothelial cell adhesion molecule 1(PECAM-1), and P-Selectin in adult mouse lungs exposed to hyperoxia that coincided with a rapid deterioration of respiratory status. In the present study, we will compare the gene expression of ICAM-1, PECAM-1, and P-Selectin in the lungs of newborn mice exposed to 100% O-2 for 4, 7 or 10 days. Age-matched animals exposed to room air will serve as control. Cellular adhesion molecule (CAM) mRNA expression was assessed by in situ hybridization. In control animals, only PECAM-1 mRNA was detected in the endothelium of large arteries with a slight increase at 10 days. ICAM-1 mRNA was not detected before 7 d of hyperoxia, whereas it was abundantly expressed in the alveoli and airway epithelium. A marked increase in PECAM-1 mRNA expression was also seen in endothelial cells, and alveoli after 7 d of hyperoxia. In contrast, only barely detectable P-Selectin mRNA was observed in the endothelial cells of large vessels of the same animals. Both ICAM-1 and PECAM-1 expression appeared maximum at 7 days of hyperoxia. In contrast to the adult mouse, the increase in CAMs expression occurred later and was not associated with lethal lung damage. Moreover, the increase in PECAM-1 mRNA was higher than in the adults, but P-Selectin increase was smaller. We speculate that the induction of some CAMs during hyperoxia could be beneficial by promoting the healing process.

Support: Québec Pulmonary Association, Telethon de la Recherche sur les maladies infantiles, and Fond de Recherche en Sante du Quebec.