Can fluid be reabsorbed from flooded rabbit lungs?

Details

The mechanisms that clear fluid from air spaces flooded during severe pulmonary edema remain uncertain. Researchers investigated solute and water fluxes in isolated, fluid-filled, perfused rabbit lungs. They perfused the lungs with physiologic albumin solutions of 1.0 or 5.0 g/dl and flushed and filled the air spaces with the same solutions. They sampled the perfusate at intervals and, after 1 or 2 hours, pumped fluid from the trachea into collection tubes.

Air-space concentrations of albumin labeled with Evans blue increased by 2.4 ± 0.7% at 1 hour and 7.0 ± 0.8% at 2 hours; the uncertainty is the standard error of the mean (SEM). About half of the increase at 2 hours could be attributed to dehydration, judged from increases in sodium concentration in the perfusate and air spaces. Previous studies indicated that labeled protein moves very slowly between these compartments in this preparation, so the researchers concluded that fluid was being reabsorbed from the air spaces. Reabsorption appeared slower in rabbits than in rats and was not stimulated by terbutaline, unlike an effect observed in other species.

Under control conditions, air-space fluid potassium concentration fell from 4.01 ± 0.05 to 3.37 ± 0.14 mEq/L at 1 hour, with uncertainty reported as SEM. Over the same interval, perfusate potassium rose from 3.95 ± 0.05 to 4.39 ± 0.08 mEq/L. Air-space potassium also decreased and perfusate potassium increased over 2 hours when the lungs were perfused with the 5 g/dl albumin solution. Adding 10−5 M terbutaline to the airway and perfusion solutions increased air-space potassium from 3.97 ± 0.05 to 4.49 ± 0.13 mEq/L. This terbutaline effect was largely blocked by 10−5 M propranolol.

The researchers suggested that forces other than hydrostatic pressure or differences in protein concentration may transport fluid out of rabbit lung air spaces. They also suggested that electrolyte transport across the pulmonary epithelium may differ between species.