Résumé
PURPOSE: In the treatrnent of respiratory distress syndrome, Infants are often exposed to hyperoxia. It can generate oxygen free radical, damage to lung and bronchi, and inactivate pulmonary surfactant(PS). Antioxidant therapy in animal and human models has been tried to overcome this detrimental effects. We hypothesized that the addition of oxygen free radical such as hydrogen peroxide(H) could compromise surface active properties(SAP) of PS and that further addition of antioxidant such as catalaseR(CAT, Sigma chemical, St. Louis) could recover SAP. METHODS: We prepared combinations of mixtures with SurfactenR(S-TA, Tokyo Tanabe, Japan), H202 and CAT. 1)0.625mgPL(phospholipids)/ml or 1.25mgPL/ml S - TA and H202 were mixed to the final concentrations of 0.1 and 1mM H respectively, and incubated at 37C for one hour. 2) 0.625mgPL/rnl S - TA, H202 and CAT 10U were mixed to the final concentrations of lmM H202, and incubated at 37 degree C for one hour. We used Pulsating Bubble Surfactometer (Electronetics, NY) measure in vitro minimum and maximum surface tensions(ST) and area-surface tension relationship. RESULTS: 1) For 0.625mgPL/ml S-TA and 1mM H mixture minimum. ST after 5 min of pulsation increased significantly(P=0.007) and the area-surface tension curve was deformed. But they were comparable to control levels for 1.25mgPL/ml S-TA. 2) When CAT was added to 0.625mgPL/ml S-TA and 1mM H mixture, the resultant minimum ST after 5 min of pulsation dropped to the control levels with recovery of hysteresis curve(P=0.0001). CONCLUSION: PS could be inactivated by addition of high concentrations of H but SAP can be recovered either by increasing PS concentration or by further addition of antioxidant CAT. Therefore, we suggest that in case of suspected surfactant inactivation an increase in surfactant concentration or administration of antioxidant must be considered.