Low molecular weight dextran attenuates increase in extravascular lung water caused by ARDS.

We studied the effect of low molecular weight dextran (mean molecular weight 40,000, Dextran 40; LMD) on the accumulation of extravascular lung water (EVLW), and also on hemodynamics and blood gases, in the oleic acid (OA)-injured lung in pentobarbital anesthetized rats. Starting just before the OA injection (0.01 mL/kg via femoral vein), 10% LMD in lactated Ringer's solution was infused throughout the experiment (5 mL/kg/h) instead of lactated Ringer's solution. OA caused acute lung injury leading to decreased oxygenation (PaO2: 87 +/- 11 mmHg versus control group 128 +/- 11) and an increased permeability of the alveolar-capillary membrane, as shown by increases in EVLW (4.89 +/- 0.54 versus control group 4.07 +/- 0.14), and albumin leakage (0.043 +/- 0.015 versus control group 0.010 +/- 0.004). LMD protected against the increase in EVLW (4.14 +/- 0.10) and the hypoxemia (112 +/- 19 mmHg), but it did not reduce the albumin leakage into the alveolar space (0.052 +/- 0.009). These data suggest that LMD may limit the fluid accumulation that is secondary to OA-induced lung injury.