Fig. 1.

A: rosiglitazone (RGZ) prevented hyperoxia-induced aberrations in lung architecture. Seven-day continuous hyperoxia (95% O₂) exposure alone caused failure of secondary septation of distal lung air sacs resulting in larger than normal alveoli denoted by asterisks, with marked decrease in interstitial thickness (arrows). These changes were prevented by administration of RGZ (1 and 3 mg/kg ip) concomitant to hyperoxia exposure. Representative hematoxylin-eosin-stained lung sections are shown (magnification, ×40; bar, 20 μm; n = 6). B: morphometric changes of lungs in hyperoxia without and with RGZ treatment. RGZ prevented 7-day hyperoxia (95% O₂)-induced decrease in lung alveolar septal thickness, radial alveolar count, alveolar tissue density, and the accompanying increase in mean linear intercept. Significant changes in all of these parameters were observed on exposure to 95% hyperoxia alone, which were prevented by RGZ treatment (*P < 0.05, 95 vs. 21% O₂ and **P < 0.05, 95% O₂ + RGZ vs. 95% O₂ only; n = 6). C: visualization of neutrophils influx in lung of rat pups exposed to 95% O₂. Representative myeloperoxidase antibody-stained lung sections (5 μm) are presented. Myeloperoxidase-reactive neutrophils (with characteristic polylobulated nucleus) are seen in hyperoxic alveoli, which are absent in normoxic and RGZ treated lungs. Magnification, ×1,000; arrows point to the myeloperoxidase reactive neutrophils; calibration bar = 20 μm; n = 4.