Aerosolized surfactant and dextran for experimental acute respiratory distress syndrome caused by acidified milk in rats

Background:  Inhibition of pulmonary surfactant by plasma-derived proteins is an important pathogenetic factor of acute respiratory distress syndrome (ARDS). Inhalation of aerosolized surfactant may be suitable for early treatment of ARDS. However, requirement of a high dose is a drawback. Because dextran reverses surfactant inhibition, we examined whether dextran improves the therapeutic effects of aerosolized surfactant in rats with experimental ARDS. Methods:  Acidified milk (pH 1.8, 1.5 ml kg−1) was injected into the trachea of the rats ventilated with pure oxygen using 2.45 kPa peak inspiratory pressure and 0.74 kPa positive end-expiratory pressure. When PaO2 decreased to <13 kPa, the rats were assigned to four groups: control group (n = 8), receiving no material; D-only group (n = 6), receiving aerosolized dextran for 45 min; S-only group (n = 8), receiving aerosolized modified natural surfactant (MNS) for 30 min; and S-plus-D group (n = 9), receiving aerosolized MNS for 30 min followed by aerosolized dextran for 15 min. Results:  In the control group and D-only groups, the mean PaO2 remained at 38 kPa for 180 min (P < 0.01 vs. S-only group). Conclusion:  Inhalation of aerosolized dextran potentiates the effects of aerosolized surfactant by prolonging the therapeutic response.