Introduction: Experimental models of acute lung injury treated with partial liquid ventilation (PLV) exhibit attenuation in tissue damage and inflammation. We have previously shown a decrease in free radical release by alveolar macrophages1 exposed to PFOB and attenuation in oxidative injury to the lung in animals treated with PLV2. Considering the lipophilic properties of PFOB and that lipid peroxidation products, such as MDA, are capable of augmenting tissue injury, we hypothesized that PFOB might solubilize MDA, thus reducing the concentration of MDA in the aqueous phase and attenuating the degree of MDA-induced tissue injury. Methods: Known concentrations of MDA (2.5 to 20 μM) were placed in glass tubes and incubated at 25°C in the absence (control) or presence of PFOB (PFOB) during constant agitation for 1 h. MDA concentrations were assayed in the aqueous and PFOB phases by the method of Esterbauer and Cheeseman: the sample was added to a solution of 10.3 mM N-methyl-2-phenylindole in acetonitrile and methanol, acidified with 37% HCl and incubated at 45°C for 1 h. Absorbance was measured at 586 nm with a spectrophotometer. Results: Bars represent means ± SD for samples obtained from the aqueous phase. No MDA was recovered from the PFOB phase. Conclusions: PFOB does not act as a reservoir for MDA. The attenuation in oxidative damage observed in experimental models of PLV is not due to adsorption of lipid peroxidation products away from direct contact with tissues.
|Original language||English (US)|
|Journal||Critical Care Medicine|
|Issue number||1 SUPPL.|
|State||Published - 1999|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine