Effect of hyperbaric and normobaric oxygen on pulmonary endothelial cell function.

The effect of prior exposure to raised partial pressures of oxygen on pulmonary endothelial cell function was assessed in the isolated perfused rat lung preparation. Prolonged exposure to both 1 bar (48 h) and 2.5 bar (11 h) of oxygen caused pulmonary edema and dyspnea. Exposure to 1 bar oxygen for 48 h (approximately 0.66 lethal duration) caused a decrease in pulmonary 5-hydroxytryptamine (5-HT) clearance, suggesting compromised endothelial cell integrity. No change in 5-hydroxy-indole acetic acid (5-HIAA) efflux was noted. However, exposure to 2.5 bar of oxygen for up to 11 h (approximately 0.85 lethal duration) did not decrease pulmonary 5-HT clearance, implying that endothelial cell integrity was not compromised after this oxygen exposure. Exposure to 2.5 bar oxygen resulted in a reduction in 5-HIAA efflux, possibly indicating a decrease in metabolism of cleared 5-HT. The absence of a demonstrable impairment of 5-HT clearance during the development of pulmonary toxicity on exposure to 2.5 bar of oxygen suggests that there may be important differences in pathologic mechanisms in response to oxygen exposure at partial pressures 1 and 2.5 bar.