Ueda T, Ikegami M
Department of Pediatrics, Harbor-UCLA Medical Center, Torrance, California 90509, USA.
Am J Respir Crit Care Med. 1996 Jun;153(6 Pt 1):1844-9. doi: 10.1164/ajrccm.153.6.8665044.
We asked if the function of surfactant could be enhanced after exposure to injured lungs. We also asked if sensitivity to inhibition of the minimal surface-tension-lowering properties of surfactant by plasma could be altered. Lung injury in rabbits was induced with N-nitroso-N-methylurethane (NMU) and 6 of 17 NMU-injured rabbits were treated with 100 mg/kg surfactant. All rabbits were ventilated for 2 h, and large aggregate alveolar surfactant was isolated by centrifugation. In vivo function of the large aggregate surfactant was evaluated by treatment of preterm surfactant-deficient rabbits at 27 d gestation. Surfactant from NMU-injured lungs increased compliance from 0.37 +/- 0.01 in control preterm rabbits to 0.71 +/- 0.05, a value significantly higher than found for the surfactant used for treatment (0.55 +/- 0.04) (p < 0.05). The minimal surface tensions of large aggregate surfactant and the surfactant used for treatment (0.1 mg lipid/ml) were evaluated for inhibition by plasma proteins. Surfactant from NMU-injured and surfactant-treated rabbits was more resistant to inhibition (minimal surface tension, 5.7 +/- 3.9 dyne/cm in the presence of 0.6 mg/ml plasma protein) than the surfactant used for treatment (19.7 +/- 0.8 dyne/cm). These results indicate that after exposure to the injured lung, the function of the surfactant used for treatment was enhanced and made less sensitive to plasma inhibition of the surface-tension-lowering properties of surfactant. These changes probably result from the association of endogenous surfactant components with exogenous surfactant.