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1 Department of Physiology and Pharmacology, Lawson Health Research Institute, University of Western Ontario, London, Ontario, Canada
2 Department of Physiology and Pharmacology, Lawson Health Research Institute, University of Western Ontario, London, Ontario, Canada; Department of Medicine, University of Western Ontario, London, Ontario, Canada
3 Department of Biochemistry, University of Western Ontario, London, Ontario, Canada
* To whom correspondence should be addressed. E-mail: tbailey2{at}uwo.ca.
Pulmonary surfactant is a mixture of phospholipids (~90%) and surfactant associated proteins (SP's) (~10%) that stabilize the lung by reducing the surface tension. One proposed mechanism by which surfactant is altered during acute lung injury is via direct oxidative damage to surfactant. In vitro studies have revealed that the surface activity of oxidized surfactant was impaired and that this effect could be overcome by adding SP-A. Based on this information, we hypothesized that animals receiving oxidized surfactant preparations would exhibit an inferior physiologic and inflammatory response and the addition of SP-A to the oxidized preparations would ameliorate this response. To test this hypothesis mechanically ventilated, surfactant deficient rats were administered either bovine lipid extract surfactant (BLES) or in vitro oxidized BLES of three doses; 10mg/kg, 50mg/kg or 10mg/kg + SP-A. When instilled with 10mg/kg normal surfactant the rats had a significantly superior PaO2 responses compared to the rats receiving oxidized surfactant. Interestingly, increasing the five times dose mitigated this physiologic effect and the addition of SP-A to the surfactant preparation had little impact on improving oxygenation. There were no differences in alveolar surfactant pools and the indices of pulmonary inflammation between the 10mg/kg dose groups, neither was there any differences observed between either of the groups supplemented with SP-A. However, there was significantly more surfactant and more inflammatory cytokines in the 50mg/kg oxidized BLES group compared to the 50mg/kg BLES group. We conclude that instillation of an in vitro oxidized surfactant causes an inferior physiologic response in a surfactant deficient rat.
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